Motivation and emotion/Book/2016/Parkinson's disease treatment motivation

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Parkinson's disease treatment motivation:
How does motivation to decrease PD symptomatology affect the efficacy of treatment?

Overview[edit | edit source]

How does motivation to decrease Parkinson's disease (PD) symptomatology affect the efficacy of treatment? In this chapter, that is the perennial question, with its ultimate goal being to understand motivation in PD. Furthermore, this chapter will outline the stages of pathological development, including a basic understanding of treatments and physiological mechanisms that affect motor function in PD. In the second half of this chapter, exploring motivational concepts such as self-efficacy and hope, and their relation to PD, will build a synthesis toward an educational resource for PD individuals.

Learning outcomes

  1. To understand what PD is, and its development.
  2. Understand the role of dopamine in PD.
  3. An overview of the common treatments for PD.
  4. Understand the motivational concepts of self-efficacy and hope, including their role in PD.

What is Parkinson's disease (PD)?[edit | edit source]

PD is an incurable progressive neurodegenerative disease, primarily known for its impairment to motor function (Jankovic, 2008; NINDS, 2016). The four primary motor symptoms of PD are tremor or trembling in the hands, arms, legs, jaw and face; muscle rigidity, bradykinesia (slowness of movement); and postural instability which can result in problems with balance and coordination (NINDS, 2016; Sveinbjornsdottir, 2016). As the disease develops, symptoms become more pronounced, leading to many problems including difficulty talking and walking, as well as neuropsychiatric symptoms including cognitive impairment (Lewy body Dementia), depression, anxiety, sleep problems and psychosis (Jankovic, 2008). There are six stages in the course of pathological development, with the latter stages 5 and 6 showing the most obvious signs such as motor symptoms (see Table 1).

Table 1.

Stages of Pathological development in Parkinson's disease.

Stages of pathological development in Parkinson's disease.


Clinical symptoms

  • Stages 3-4 (Jankovic, 2008; Sveinbjornsdottir, 2016): Lewy bodies start to form in the forebrain and midbrain areas. Degeneration and Lewy bodies start to appear in the dopamine nerve cells of the basal ganglia and substantia nigra. Degeneration of the dopaminergic nigrostriatal neurons constitute the primary feature of motor dysfunction in PD. Symptoms include: tremor, rigidity, bradykinesia and postural instability.
  • Note: Research suggests (e.g., Sveinbjornsdottir, 2016) that clinical symptoms manifest at this stage, although evidence is often hard to verify. This is often because individuals with PD do not present for clinical assessment until degeneration has impaired their standard of living; stages 5 and 6.
  • Stages 5-6 (Jankovic, 2008; Sveinbjornsdottir, 2016): At this stage abnormalities become apparent in the neocortex, which is involved in higher order functioning such as sensory perception, motor commands, spatial reasoning and language. Neurodegeneration may also be apparent in other neural pathways, giving rise to previously mentioned neuropsychiatric symptoms.
  • At this stage both motor and non-motor symptoms are present.

The role of dopamine in PD[edit | edit source]

Dopamine plays an integral role in the physiological motivation of controlled motor movement in the body (Jankovic, 2008). Along this line, the loss of dopamine facilitating neurons in the substantia nigra, disturbs normal neurological functioning, changing a person's physical control over motor movements (Jankovic, 2008). As neurons start to degenerate in the substantia nigra, its role as a facilitator for movement readiness also starts to diminish (Kalat, 2014). The loss of dopamine-releasing axons means there is also a loss of axons to the ventral striatum, which is strongly associated with reward, risk and decision making (Kalat, 2014). As a consequence of losing these neural connections, the ventral striatum, decreases its inhibition of the globus pallidus, which is responsible for the regulation of voluntary movement, working closely with the cerebellum to create smooth controlled movement (Kalat, 2014). In turn, the globus pallidus inhibits the thalamus which communicates sensory motor information between the sub-cortical areas and the cortex (Kalat, 2014).

The end result? People with PD are still capable of controlled movement, but a communication breakdown in dopamine facilitating pathways, causes involuntary movement problems such as tremor, poor balance and coordination (NINDS, 2016). It can also result in voluntary movement issues such as "freezing" (hypokinesia), and gait problems such as slowness of movement (Sveinbjornsdottir, 2016).

Treatments[edit | edit source]

In consideration of treating a complicated disease such as PD, a few background issues should first be addressed. Firstly, PD has no cure with most treatments seeking to improve the daily functioning of PD sufferers (Cools, 2006). Secondly, and as addressed in the 'Stages of pathological development' section (see Table 1), the degeneration of dopamine nerve cells mean that as the disease progresses treatments become less effective (Jankovic, 2008). As a result of this, pharmacological treatments such as Levodopa (L-dopa), decrease in effectiveness, but still remain the primary and most effective treatment for managing PD (Cools, 2006; Jankovic, 2008; Sveinbjornsdottir, 2016). Furthermore, as PD progresses, physiotherapy and invasive neurosurgical treatments such as Deep Brain Stimulation (DBS) [missing something?] name some of the interventions used to treat PD (Cools, 2006).

Figure 1. Visible tremor, an uncontrollable movement commonly found in the hand, initiated from the contralateral side of the brain most affected by Parkinson's disease.

On a motivational level, treatments seek to reestablish normal physiological regulation, which in turn gives rise to re-energised and goal directed motor movement (Dempsey, 1951; Fahn, 2008). Furthermore, with the help of medication or neurosurgical intervention, an individuals[grammar?] physiological needs can be met (Jankovic, 2008). However, for any treatment to be effective, adherence to a treatment plan is the most important component to intervention (Leopold, Polansky, & Hurka, 2004). Moreover, high-hope and self-efficacy can improve motivation and persistence in a treatment plan.

Levodopa (L-dopa)[edit | edit source]

In the management of PD, L-dopa, the chemical precursor to the neurotransmitter dopamine, is the gold standard for management of PD (NINDS, 2016). The biggest reason L-dopa has been so effective, has been its ability to bypass the blood brain barrier, replenishing the brains[grammar?] dwindling supply of dopamine (Cools, 2006; Hornykiewicz, 2002). The replenishment of dopamine in areas such as the substantia nigra, means that there is more dopamine available to facilitate movement (NINDS, 2016). As a result, L-dopa primarily increases daily function by reducing the severity of symptoms such as bradykinesia, rigidity and, in some cases, tremor (Fahn, 2008, NINDS, 2016). Concurrently, carbidopa and other agonists are used in conjunction with L-dopa, delaying the metabolism of dopamine, and thereby increasing the availability of dopamine in degenerated dopaminergic nerve cells (Fahn, 2008; NINDS, 2016).

While L-dopa can increase physiological motivation, over the longer term it can have side effects including extreme emotional reactions, particularly anxiety, and increased motivational states such as increased libido (Cools, 2006; Fahn, 2008). Furthermore, as L-dopa and carbidopa dosages are increased due to the degeneration of dopamine nerve cells, severe on-state (see Table 2.) side effects can see increased Dyskinesia, which are the involuntary muscle movements found in PD (Cools, 2006; see Figure 1). Additionally, prolonged exposure to L-dopa medication can result in Dopamine dysregulation syndrome, which disrupts the reward system of the brain; leading to motivational self-control problems such as gambling, increased sexual behaviour, and addiction to medication (Merrims & Giladi, 2008). At this stage, when dopamine responsive therapies such as L-dopa lose their efficacy, or in young onset PD where the prognosis for PD symptomatology is substantially worse, more invasive treatments may be deemed more appropriate (Schrag, Hovris, Morley, Quinn, & Jahanshahi, 2003).

Table 2.
L-dopa and the On-Off Phenomenon.

The On-off phenomenon
The on-off phenomenon is an almost unavoidable side effect of L-dopa medication, creating fluctuations between medication working and not working (Lees, 1989). In the on-state, individuals are said to be under the effects of medication or medication is working; and in the off-state, individuals are either off the medication or medication is non-responsive (Lees, 1989). Where the problems occur, and where the on-off phenomenon is seen, is that long term exposure often creates fluctuations in the responsiveness of L-dopa, meaning one moment medication allows for control over motor movements, and the next control is gone (Lees, 1989). Along with this, fluctuations which result because of dopamine nerve cell degeneration, can lead to higher dosages of L-dopa, causing in the longer term side effects such as Dopamine Dysregulation Syndrome (Lees, 1989; Mirrims & Giladi, 2008).

In many ways L-dopa can be like a flickering light globe, one moment the light shines brightly, and the next power short circuits, and the light begins to fade. Where L-dopa draws similarity, can be seen in what is known as the on-off phenomenon (Lees, 1989). With light emitted from the light globe being motivated and energetic movement, and the power supply being a responsive and functioning dopamine nerve cell.

Deep brain stimulation[edit | edit source]

Figure 3. Neurosurgeons prepare a patient for brain surgery. In the treatment of Parkinson's disease, neurosurgical procedures such as Deep Brain Stimulation are used to increase the quality of life for people living with Parkinson's.

Treatments for PD have progressed in small steps, with a fairly stable theory of why PD occurs, and treatments that are evolving but which are not truly understood (Jankovic, 2008). Deep Brain Stimulation (DBS) is used as the main treatment for severe cases of PD. It is an invasive surgical procedure that implants electrical stimulation technologies such as electrodes into the brain (Coffey, 2008). The insertion of electrodes deliver a constant stimulation to specific brain areas or pathways such as the dopaminergic system, mimicking the effects of L-dopa (Benabid, 2003; Coffey, 2008). Constant stimulation by electrodes in brain areas, such as the subthalamic nucleus, inhibits abnormal brain activity in other brain areas such as the substantia nigra, thalamus and globus pallidus (Benabid, 2003; Lozano, Dostrovsky, Chen, & Ashby, 2002). In doing so, stimulation seeks to increase neural plasticity to create long term changes that protect the brain, and reduce symptoms such as slowness of movement, gait problems and tremor (Lozano et al., 2002).

However, invasive surgical procedures such as DBS are not without their problems, with the average age of PD individuals being over the age of 60 (NINDS, 2016). In reality, this means patients who undergo surgery are more at risk of complications, slower rates of recovery, and death (McGwin, MacLennan, Fife, Davis, & Gregory, 2004). For PD patients, this can mean surgery may not always be the best option, with higher risks associated with aged-related comorbidites (NINDS, 2016).

Physiotherapy and neurostimulation[edit | edit source]

Physiotherapy is another treatment often used in conjunction with L-dopa to manage the day to day motor symptoms of PD, with physiotherapy aiming to reduce gait problems and other PD motor symptomology (Tomlinson et al., 2012). Exercise programs seek to increase quality of life by reducing balance problems which make PD individuals more prone to injury because of falls (Tomlinson et al., 2012). Proprioception, which is a person’s perception of their limb and trunk position in space, generated from the senses in the skin and limbs, can be improved (Waddington, Addams, Han, & Witchalls, 2015) via physical exercises which strengthen the neural connections between the motor cortex and sensory nerves, such as those found in the hands and feet (see Tango therapy in See also section; Waddington et al., 2015).

To increase the effectiveness of physical exercise on proprioception, neurostimulation techniques, such as transcranial Direct Current Stimulation (tDCS), can be effective (Nitsche et al., 2007). tDCS increases the rate of neural learning (neural plasticity), so benefits from physical exercise are accomplished with higher levels of competency or faster rates of acquisition (Broeder et al., 2015). Physiotherapy can be utilised through dance as a therapy, which can improve functional mobility and quality of life experienced by PD individuals (Kaski, Allum, Bronstein, & Dominguez, 2014). However, as is the case with the majority of PD intervention strategies, degenerating nerve cells mean the benefits of physical therapy are short lived as neural pathways between the cortex and limbs succumb to cell death (apoptosis; Tomlinson et al., 2012).

Watch Professor Rafael Eldor's 2015 TEDx talk:
Dance as a medicine for Parkinson's
7:47 mins

Motivation in the face of a chronic illness.[edit | edit source]

PD treatments seek to strengthen or replenish degenerating dopaminergic pathways (Jankovic, 2008). However, because treatments are designed to slow the progress of PD, and not cure PD, motivation to continue a treatment can leave individuals feeling deflated and uninspired (Gum & Snyder, 2003). From this, fostering hope through the strengthening of self-efficacy can lead to better coping and perhaps a more effective treatment program.

Building self-efficacy - empowering the individual to thrive in a difficult situation.[edit | edit source]

Figure 4. The internal struggle. Motivating yourself in the face of a PD diagnosis can feel like a mountain to climb.

The reality of a PD diagnosis.: Imagine you were just diagnosed with PD. You're 62, healthy, been a mechanic all your life, and you still work full-time! Your friends and family have always thought of you as the "man of the house" - a handy man, someone physically reliable. In your own eyes, your effectiveness as a man, a husband, and a father, has been in your ability to fix things with your hands. Now imagine the tremor has started, you're not sure what is going on, all you know is something isn't right. After a visit to the doctor, you're given the diagnosis. The news hasn't quite settled in yet, but its deflating and you realise that your perception of your self is going to change, and there is nothing you can do about it (see Figure 4).

This vignette paints a picture of what some people go through when given the news of a chronic illness (Gum & Snyder, 2003). In light of this, Bandura (1977) proposed that what some people were really struggling with, was their belief in relation to ability about effectively and competently dealing with the world (Bandura, 1977). Consequently, Albert Bandura's proposed the notion of self-efficacy (Bandura, 1977), which is an individual's belief in their own ability to cope effectively and deal with changing situations (Bandura, 1977). Bandura (1977) proposed vicarious experience (seeing others master tasks), physiological arousal (attribution or biofeedback), verbal persuasion (encouragement from others) and performance accomplishments (modelling behaviour based on personal history) as the four sources that give rise to self-efficacy.

A health professional who recognises the deficits to self-efficacy arising as a result of diagnosis of PD, can use these four sources of self-efficacy to help empower individuals (Ozer & Bandura, 1990). This can be done through a mastery modelling program (Ozer & Bandura, 1990), which allows improvement within themselves by learning from an expert, building skills, competence and self-efficacy (Reeve, 2015). Physical therapists can utilise their skill to help PD individuals increase their quality of life (Tomlinson et al., 2012) by strengthening physiological mechanisms such as proprioception (Tomlinson et al., 2012; Waddington et al., 2015). As a result of using mastery modelling programs, individuals can build towards higher levels of self-efficacy. In conjunction, changing their mindset to a high-hope mindset (see Snyders[grammar?] Hope Theory) can help increase psychological motivation, making the unbearable pleasant, and perhaps even enjoyable.

Self-efficacy training program[edit | edit source]

Based on Ozer and Bandura's (1990) self-efficacy mastery program:

  1. The physiotherapist identifies component skills needed for effective coping, such as balance and coordination. States the benefits of particular exercises and end results to the PD client[grammar?].
  2. The physiotherapist models how to complete each exercise, modelling areas which will be most difficult, need the most work, or unlikely to see improvement.
  3. The client emulates the exercises and the physiotherapist provides guidance and corrective feedback as needed.
  4. The client integrates the different exercises into an overall simulated performance. The physiotherapist introduces obstacles such as uneven ground, to test balance, and allows for the integration of psychological coping and physical technique.
  5. The client participates unassisted, gives a simulated performance while the physiotherapist watches. The physiotherapist provides encouragement and tips. The client repeats the performance.
  6. The client practices the exercises at home, or in a near naturalistic situation. Features realistic difficulties, such as getting out of the shower, uneven ground[grammar?]. The physiotherapist watches, providing guidance, corrective feedback, re-instruction of coping techniques as needed.
  7. The physiotherapist (or psychologist) models how to approach tasks confidently, models how to manage stress, or how to deal with off-state days when motor control is uncontrollable.

Via these steps the PD client can learn to cope better in unpredictable situations and thereby increasing their belief and ability in themselves. Moulding the anxious novice into a highly self-efficacious individual[grammar?].

Fostering hope - Snyder's Hope Theory[edit | edit source]

Snyders[grammar?] cognitive theory of hope (STH) states that utilising alternative pathways to achieve a goal can be done by approaching life with sense of self-belief or agency (Gum & Synder, 2003). In turn, building self-efficacy and agency towards those pathways allows hope to be fostered (Gum & Synder, 2003). For people living with an incurable disease, the use of positive psychological applications such as STH, allow PD sufferers to develop positive coping mechanisms (Gum & Synder, 2003). Furthermore, applying STH can foster a sense of hope by allowing for positive thoughts that look beyond the physical detriments of motor dysfunction (Gum & Snyder, 2003). Depending on whether the person see the glass as half-full (high-hope person) or half-empty (low-hope person), the pathways to goal attainment can be seen as insurmountable or a challenge to be conquered (Gum & Snyder, 2003; Snyder, 2002).

Individuals who have a high-hope outlook on life tap into their intrinsic motivational resources of confidence, optimism, self-efficacy, and mastery belief (Gum & Snyder, 2003; Snyder, 2002). Meaning when they are faced with situational circumstances where the outcomes are bleak (e.g., diagnosis of PD), they are more likely to find motivational support (Gum & Snyder, 2003; Snyder et al., 1991)[grammar?]. Furthermore, they are more likely to persist longer toward a desired goal, have a higher sense of agency, and use alternate pathways such as mastery goals to overcome difficulties, such as a diagnosis of PD (Gum & Snyder, 2003). However, for individuals who foster a low-hope outlook on life, they do not persist as long, have difficulty choosing alternate pathways, and are more likely under perform compared to an individual who fosters high-hope or glass half full lease on life (Snyder, 2002; Snyder et al., 1991). In light of this, high-hope individuals are more likely to find a solution to a difficult task or persevere with a treatment plan as they come to grips with an incurable diagnosis (Gum & Snyder, 2003).

How hopeful are you? Click the Snyder adult hope scale to measure your levels of hope (Snyder et al., 1991).

High-hope individuals out perform and have better coping strategies than low-hope individuals[edit | edit source]

Why do high-hope individuals out perform and have better coping strategies than individuals with a low-hope mindset? High-hope people (Snyder, 2002):

  1. implement short term goals, by breaking down larger goals into smaller ones.
  2. utilise mastery goals, which focus on the understanding of material, the learning process and mastery of concepts (compared to achievement goals which focus on outcome only).
  3. rely on internal self-set goals.
  4. engage in goals that are intrinsically motivating rather than extrinsically motivating.
  5. adopt flexible approaches to problem solving, reducing functional fixedness.
  6. are intrinsically motivated which increases determination and task persistence.
  7. enjoy the process rather than the outcome, and see the positive rather than negatives of a situation.

Conclusion[edit | edit source]

Motivation plays a physiological and psychological role in PD treatment. Research indicates that PD treatments seek to mimic or repair the degeneration of dopaminergic neurons, which facilitate readiness for movement. Physiotherapy can also be used to improve an individuals[grammar?] day to day quality of life. Self-efficacy and hope can also be enhanced and play a key role in motivating an individual in the face of a chronic disease. Self-efficacy can be built through mastery building programs and learning to think more positively about one's ability to cope in difficult situations. Self-efficacy helps to boost hope. High-hope individuals persist longer with tasks, and are more likely to seek motivational support, thereby increasing their intrinsic motivation for, and likely continuation of, a treatment plan. However, despite the good intentions of motivation, fostering hope and self-efficacy make treatments no more or less effective. Meaning[grammar?][Rewrite to improve clarity], being a highly self-efficacious and highly hopeful individual will allow you to better cope and come to terms with a disease, but have no baring on the reduction of symptomology or the efficacy of treatment.

See also[edit | edit source]

  1. Book chapter (2014): Dopamine and motivation.
  2. Book chapter (2011): Self-efficacy and motivation.
  3. Book chapter (2015): TDCS and Motivation.

References[edit | edit source]

Bandura, A. (1977). Self-efficacy: toward a unifying theory of behavioral change. Psychological review, 84(2), 191. doi:10.1037/0033-295X.84.2.191

Benabid, A. L. (2003). Deep brain stimulation for Parkinson’s disease. Current opinion in neurobiology, 13(6), 696-706. doi:10.1016/j.conb.2003.11.001

Broeder, S., Nackaerts, E., Heremans, E., Vervoort, G., Meesen, R., Verheyden, G., & Nieuwboer, A. (2015). Transcranial direct current stimulation in Parkinson's disease: Neurophysiological mechanisms and behavioral effects. Neuroscience & Biobehavioral Reviews, 57, 105-117. doi:10.1016/j.neubiorev.2015.08.010

Coffey, R.J. ( 2009). Deep brain stimulation devices: a brief technical history and review. Artificial. Organs, 33(3), 208–20. doi:10.1111/j.1525-1594.2008.00620

Cools, R. (2006). Dopaminergic modulation of cognitive function-implications for l-DOPA treatment in Parkinson's disease. Neuroscience & Biobehavioral Reviews, 30(1), 1-23. doi:10.1016/j.neubiorev.2005.03.024

Dempsey, E.W. (1951). Homoeostasis. In S.S. Stevens (Ed.), Handbook of experimental psychology (pp. 209-235). New York: Wiley.

Fahn, S (2008). The history of dopamine and levodopa in the treatment of Parkinson's disease. Movement Disorders, 233, 497–508. doi:110.1002/mds.22028

Gum, A., & Snyder, C. R. (2002). Coping with terminal illness: The role of hopeful thinking. Journal of palliative medicine, 5(6), 883-894. doi:10.1089/10966210260499078.

Han, J., Anson, J., Waddington, G., Adams, R., & Liu, Y. (2015). The role of ankle proprioception for balance control in relation to sports performance and injury. BioMed Research International, 1-8. doi:10.1155/2015/842804

Hornykiewicz, O. (2002). L-DOPA: from a biologically inactive amino acid to a successful therapeutic agent. Amino Acids, 23(1–3), 65–70. doi:10.1007/s00726-001-0111-9.

Jankovic, J. (2008). Parkinson’s disease: clinical features and diagnosis. Journal of Neurology, Neurosurgery & Psychiatry, 79(4), 368-376. doi:10.1136/jnnp.2007.131045.

Kalat, J.W. (2014). Movement disorders (12th eds.). In Biological Psychology (pp. 227-260). Retrieved from;jsessionid=2C52BEC022EBD4C36B9F6E3E5032B606?N=16+4294962964+4294963756&Ntk=P_EPI&Ntt=168990977981667418819972126601870960342&Ntx=mode%2Bmatchallpartial

Kaski, D., Allum, J. H., Bronstein, A. M., & Dominguez, R. O. (2014). Applying anodal tDCS during tango dancing in a patient with Parkinson's disease. Neuroscience letters, 568, 39-43. doi:10.1016/j.neulet.2014.03.043

Lees, A. J. (1989). The on-off phenomenon. Journal of Neurology, Neurosurgery & Psychiatry, 52, 29-37. doi:10.1136/jnnp.52.Suppl.29

Leopold, N. A., Polansky, M., & Hurka, M. R. (2004). Drug adherence in Parkinson's disease. Movement Disorders, 19(5), 513-517. doi:10.1002/mds.20041

Lozano, A. M., Dostrovsky, J., Chen, R., & Ashby, P. (2002). Deep brain stimulation for Parkinson's disease: disrupting the disruption. The Lancet Neurology, 1(4), 225-231. doi:10.1016/S1474-4422(02)00101-1

McGwin Jr, G., MacLennan, P. A., Fife, J. B., Davis, G. G., & Rue III, L. W. (2004). Preexisting conditions and mortality in older trauma patients. Journal of Trauma and Acute Care Surgery, 56(6), 1291-1296.

Merims, D., & Giladi, N. (2008). Dopamine dysregulation syndrome, addiction and behavioral changes in Parkinson's disease. Parkinsonism & related disorders, 14(4), 273-280. doi:10.1016/j.parkreldis.2007.09.007

Nitsche, M. A., Doemkes, S., Karakoese, T., Antal, A., Liebetanz, D., Lang, N., ... & Paulus, W. (2007). Shaping the effects of transcranial direct current stimulation of the human motor cortex. Journal of neurophysiology, 97(4), 3109-3117. doi:10.1152/jn.01312.2006

Ozer, E. M., & Bandura, A. (1990). Mechanisms governing empowerment effects: a self-efficacy analysis. Journal of personality and social psychology, 58(3), 472.

Parkinson's Disease Information Page. NINDS. June 30, 2016. Retrieved from NINDS website:

Reeve, J. (2015). Understanding motivation and emotion. New York: Wiley.

Schrag, A., Hovris, A., Morley, D., Quinn, N., & Jahanshahi, M. (2003). Young‐versus older‐onset Parkinson's disease: Impact of disease and psychosocial consequences. Movement Disorders, 18(11), 1250-1256. doi:10.1002/mds.10527

Schulz-Schaeffer, W.J. (2010).The synaptic pathology of alpha-synuclein aggregation in dementia with Lewy bodies, Parkinson's disease and Parkinson's disease dementia Acta Neuropathology, 1(2). 131–43. doi:10.1007/s00401-010-0711-0

Snyder, C. R. (2002). Hope theory: Rainbows of the mind. Psychological Inquiry, 13249-275. doi:10.1207/S15327965PLI1304_01

Snyder, C. R., Harris, C., Anderson, J. R., Holleran, S. A., Irving, L. M., Sigmon, S. T., ... & Harney, P. (1991). The will and the ways: development and validation of an individual-differences measure of hope. Journal of personality and social psychology, 60(4), 570. doi:10.1037/0022-3514.60.4.570

Sveinbjornsdottir, S. (2016), The clinical symptoms of Parkinson's disease. Journal of Neurochemistry. doi:10.1111/jnc.13691

Tomlinson, C. L., Patel, S., Meek, C., Herd, C. P., Clarke, C. E., Stowe, R., ... & Ives, N. (2012). Physiotherapy intervention in Parkinson’s disease: systematic review and meta-analysis. BMJ, 345(5004). doi:10.1136/bmj.e5004

Waddington, G., Adams, R., Han, J., & Witchalls, J. (2015). Measurement of dynamic proprioception. A systematic review of the literature. Physiotherapy, 101(1594-1595). doi:10.1016/

Wu, S. S., & Frucht, S. J. (2005). Treatment of Parkinson’s Disease: What’s on the Horizon?. CNS Drugs, 19(9), 723-743. doi:10.2165/00023210-200519090-00001

External links[edit | edit source]