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Action Initiation is a form of executive function, which relates to how we cognitively begin an action. It should be noted that action initiation is not the same as premovement neuronal activity, which is related to the activity of neurons in the body.

As an executive function

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Executive functions are defined as processes that combine cognitive thoughts with actions, and enable the ability to work towards goals [1]. To begin an action, there first needs to be an intention, which gives the action a goal direction. Some actions are automatic, and therefore the person does not need to do anything to do this, such as breathing. Other actions require willful intentions from the person, such as beginning to walk. If action initiation deficits are evident, they are often more salient in actions that need willful intentions [2][3]. It is important to note that a person may not show deficits in all actions requiring willful intentions; they may only show deficits for certain actions.

Psychological inertia

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Psychological inertia is a theory derived from physics, and is defined as the tendency for things to remain in their current state, so an object in motion will continue the motion. To apply this to the context of humans, if a person has been sitting on a sofa all day they may then struggle to get up and start another activity [4][5].

This is linked to action initiation; however, there is a clear distinction between the two. Psychological inertia is related to moving out of a state, whereas action initiation is related to moving to a new state.

Neuroanatomical causes

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Action initiation processes are located in the frontal lobe of the brain [6], more specifically, the dorsolateral prefrontal cortex [7]. Further links have been shown to the basal ganglia, due to the dopaminergic pathways between the frontal lobe and the basal ganglia [8][9].

A specific structure of the basal ganglia, the globus pallidus, has a reported role in action initiation, and is effected by dopamine levels. This structure modulates inhibitory control of the cortex, and when this control is reduced, actions occur [10]. It has been suggested that deficits in action initiation in Parkinson's Disease are produced by a lack of dopamine in the basal ganglia, due to a degeneration in dopaminergic neurons, which then effect the dopaminergic pathways to the frontal lobe [11].

With regards to action initiation deficits in people with Schizophrenia, the cause may differ depending on the symptoms exhibited, as these may have an impact on dopamine levels. Negative symptoms are often associated with reduced dopamine, whereas positive symptoms are linked with excessive levels of dopamine [12]. Therefore, if a person with negative symptoms experiences initiation deficits, its likely cause is the low dopamine levels. However, if the person has positive symptoms, it is likely that they will be given dopamine-blocking medication, which will then reduce dopamine levels, and may cause action initiation deficits.

Associated conditions

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There are several conditions in which, if a person is diagnosed, they may exhibit deficits action initiation. These include Parkinson's Disease, Schizophrenia, and Depression, as well as others.

Parkinson's Disease

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Parkinson's Disease is the key condition in which people display difficulties with action initiation. When discussing Parkinson's Disease, the term freezing is used instead of action initiation [13]. An example of this is when a person with Parkinson's Disease freezes and stops while walking, and then has difficultly re-starting the motion. The person knows how to complete the movement and that they need to move, but cannot physically continue to move their legs. This shows the motor component of freezing. However, there is also a cognitive aspect to freezing and action initiation, which can often be seen when a person with Parkinson's Disease walks a route involving corners. When this happens, they are unable to use the cognitive processes necessary to work out how to turn the corner before continuing walking [14]. At this point it is not purely a motor deficit as they are physically able to walk. It has been reported that people with Parkinson's Disease have difficulties with willful intentional actions rather than automatic actions, and therefore may experience difficulty when walking a route that involves turns, or a route that features many doorways. This also explains reports of people with Parkinson's Disease being able to escape from a burning building quickly, but display symptoms again once safe [15].

Action initiation deficits in Parkinson’s Disease do not always include a motor component. For example, if a neurotypical person was asked to name as many foods beginning with the letter ‘B’ as they could in a minute, they would likely provide a list of answers. However, if a person with Parkinson’s Disease was asked to do this, they may either produce no answers due to an initiation deficit in the processes needed to think of, or name, the foods, or they may be able to produce one or two answers, but at a much slower speed [16].

Schizophrenia

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As a condition, Schizophrenia has similarities with Parkinson’s Disease, with both having links to dopaminergic pathways, and both producing deficits in action initiation [17]. In people with Schizophrenia, this may manifest in the form of poverty of speech, or alogia – a lack of unprompted speech [18]. In these cases, the person may be able to respond to questions but not produce spontaneous speech.

Depression

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Action initiation deficits can become evident in people diagnosed with depression, which is comorbid with schizophrenia [19]. With regards to depression, people develop a lack of motivation, which can therefore affect actions initiated by willful intentions [20]. This can become apparent in people with severe depression who struggle to get out of bed each day, or shower.

Measurement

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There are many ways to measure and assess action initiation deficits, in both clinical and research settings. Some deficits may be easy to spot due to their physical nature, such as freezing in Parkinson’s Disease, whilst poverty of speech or difficulty getting out of bed may noticeable to the person’s family and friends, but not to the wider population. Other deficits may require clinical or cognitive testing to be seen clearly.  

Behavioural tasks

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In research settings, computerised behavioural tasks are often used to assess cognitive deficits. One example of this is a task-switching task, which aims to measure the ability to switch from one task to another in quick succession [21]. This involves being asked to complete two tasks, Task A and Task B, and the order being manipulated. If the order involves Task A or B being repeated, then the person should enter an automatic response phase as they do not need to switch between tasks. However, if the order is randomised, then difficulty may be experienced as the switch in task requires a new action to be initiated. In neurotypical populations responses are slower on the latter order, although this difference is even larger in populations with this kind of initiation.

Simple reaction time experiments can also provide an understanding of deficits in action initiation. By asking people to complete a series of tasks as fast and accurately as they can, insights can be gained into the effects caused by difficulties with initiation. For example, people with this kind of deficit often respond at a much slower rate than neurotypical people [22] [23]. Having knowledge such as this can provide support in developing mechanisms to help, e.g., if it is understood that people with action initiation deficits can respond, but may be slower, more time can be given when testing potential treatments or therapies. 

Methods to help

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Many methods that attempt to help action initiation deficits involve the use of cues (see Kinesia Paradox). In the case of Parkinson's Disease, this may come in the form of a laser cane or portable metronome. A cane such as the one previously mentioned, uses a red laser to shine a line on the ground to provide an external cue of where the person should next place their foot, and how long their stride should be. The portable metronome also provides an external cue, this time in the form of a ticking noise, which provides a rhythm to follow so one stop can be taken for each beat.

Internal cues also provide a benefit, for example a person can internally count ‘one… two… one… two…’ or internally say ‘left… right… left… right…’ in order to provide themselves with a cue while walking. However external cues provide a larger benefit to people with action initiation difficulties than internal cues, suggesting that these deficits may be related to a problem with internal cues [24]. The use of cues for initiation deficits will only be beneficial as long as they are used; if the use of these cues are stopped, then the difficulties will return.

Depending on the form the initiation deficits manifest in, the aforementioned methods may also benefit people with Schizophrenia or Depression. However, for these two conditions medical interventions may be able to regulate dopamine levels, and therefore reduce the initiation deficits.

References

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  1. ^ Miller, E. K., & Wallis, J. D. (2009). Executive function and higher-order cognition: definition and neural substrates. Encyclopedia of neuroscience, 4(99-104).
  2. ^ Takakusaki, K., Tomita, N., & Yano, M. (2008). Substrates for normal gait and pathophysiology of gait disturbances with respect to the basal ganglia dysfunction. Journal of Neurology, 255(4), 19-29.
  3. ^ Frith, C. D. (1987). The positive and negative symptoms of schizophrenia reflect impairments in the perception and initiation of action. Psychological medicine, 17(03), 631-648.
  4. ^ Walters, G. D. (2014). Lifestyle Theory. In Encyclopedia of Criminology and Criminal Justice (pp. 2937-2946). Springer New York.
  5. ^ Alós-Ferrer, C., Hügelschäfer, S., & Li, J. (2016). Inertia and Decision Making. Frontiers in psychology, 7.
  6. ^ Schall, J. D., Stuphorn, V., & Brown, J. W. (2002). Monitoring and control of action by the frontal lobes. Neuron, 36(2), 309-322.
  7. ^ Hoffstaedter, F., Grefkes, C., Zilles, K., & Eickhoff, S. B. (2013). The “what” and “when” of self-initiated movements. Cerebral cortex, 23(3), 520-530.
  8. ^ Frank, M. J. (2005). Dynamic dopamine modulation in the basal ganglia: a neurocomputational account of cognitive deficits in medicated and nonmedicated Parkinsonism. Cognitive Neuroscience, Journal of, 17(1), 51-72.
  9. ^ Dirnberger, G., & Jahanshahi, M. (2013). Executive dysfunction in Parkinson's disease: a review. Journal of neuropsychology, 7(2), 193-224.
  10. ^ Kohl, S., Aggeli, K., Obeso, I., Speekenbrink, M., Limousin, P., Kuhn, J., & Jahanshahi, M. (2015). In Parkinson’s disease pallidal deep brain stimulation speeds up response initiation but has no effect on reactive inhibition. Journal of neurology, 262(7), 1741-1750.
  11. ^ Perez‐Costas, E., Melendez‐Ferro, M., & Roberts, R. C. (2010). Basal ganglia pathology in schizophrenia: dopamine connections and anomalies. Journal of neurochemistry, 113(2), 287-302.
  12. ^ Pogarell, O., Koch, W., Karch, S., Dehning, S., Müller, N., Tatsch, K., Poepperl. G., & Möller, H. J. (2012). Dopaminergic neurotransmission in patients with schizophrenia in relation to positive and negative symptoms. Pharmacopsychiatry, 45, S36-41.
  13. ^ Giladi, N., Treves, T. A., Simon, E. S., Shabtai, H., Orlov, Y., Kandinov, B., Paleacu, D., & Korczyn, A. D. (2001). Freezing of gait in patients with advanced Parkinson's disease. Journal of neural transmission, 108(1), 53-61.
  14. ^ Moore, S. T., MacDougall, H. G., & Ondo, W. G. (2008). Ambulatory monitoring of freezing of gait in Parkinson's disease. Journal of neuroscience methods, 167(2), 340-348.
  15. ^ Frith, C. D. (1987). The positive and negative symptoms of schizophrenia reflect impairments in the perception and initiation of action. Psychological medicine, 17(03), 631-648.
  16. ^ Janvin, C. C., Aarsland, D., & Larsen, J. P. (2005). Cognitive predictors of dementia in Parkinson’s disease: a community-based, 4-year longitudinal study. Journal of geriatric psychiatry and neurology, 18(3), 149-154.
  17. ^ Fabre, D., Vehier, A., Padovan, C., d’Amato, T., & Saoud, M. (2013). Cognitive training in schizophrenia: PrACTice preparing action with contextual information. European Psychiatry, 28(8), 14-15.
  18. ^ Messinger, J. W., Trémeau, F., Antonius, D., Mendelsohn, E., Prudent, V., Stanford, A. D., & Malaspina, D. (2011). Avolition and expressive deficits capture negative symptom phenomenology: implications for DSM-5 and schizophrenia research. Clinical psychology review, 31(1), 161-168
  19. ^ Buckley, P. F., Miller, B. J., Lehrer, D. S., & Castle, D. J. (2009). Psychiatric comorbidities and schizophrenia. Schizophrenia bulletin, 35(2), 383-402.
  20. ^ Austin, M. P., Mitchell, P., & Goodwin, G. M. (2001). Cognitive deficits in depression. The British Journal of Psychiatry, 178(3), 200-206.
  21. ^ Rubinstein, J. S., Meyer, D. E., & Evans, J. E. (2001). Executive control of cognitive processes in task switching. Journal of Experimental Psychology: Human Perception and Performance, 27(4), 763.
  22. ^ Bloxham, C. A., Mindel, T. A., & Frith, C. D. (1984). Initiation and execution of predictable and unpredictable movements in Parkinson's disease. Brain, 107(2), 371-384.
  23. ^ Michely, J., Barbe, M. T., Hoffstaedter, F., Timmermann, L., Eickhoff, S. B., Fink, G. R., & Grefkes, C. (2012). Differential effects of dopaminergic medication on basic motor performance and executive functions in Parkinson's disease. Neuropsychologia, 50(10), 2506-2514.
  24. ^ Michely, J., Barbe, M. T., Hoffstaedter, F., Timmermann, L., Eickhoff, S. B., Fink, G. R., & Grefkes, C. (2012). Differential effects of dopaminergic medication on basic motor performance and executive functions in Parkinson's disease. Neuropsychologia, 50(10), 2506-2514.
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