FoG in PD overload<\/p>\n
https:\/\/journals.plos.org\/plosone\/article?id=10.1371\/journal.pone.0144986#sec020<\/a> \u00a0<\/span><\/p>\n Subtypes<\/p>\n https:\/\/jamanetwork.com\/journals\/jamaneurology\/article-abstract\/1827554<\/a><\/p>\n Goal directed vs habitual control in the BG<\/p>\n https:\/\/pubmed.ncbi.nlm.nih.gov\/20944662\/<\/a><\/p>\n https:\/\/en.m.wikipedia.org\/wiki\/u<\/a><\/p>\n It is clear that other neurotransmitters<\/a> than DA play a role in the pathophysiology of PD (Bohnen et al., 2018; Braak et al., 2004; Delaville et al., 2012; Faggiani and Benazzouz, 2017; Fornai et al., 2007; Pahapill and Lozano, 2000; Politis et al., 2014). Yet, non-DA therapeutic strategies are still difficult to develop (Fox, 2013; Freitas and Fox, 2016). It is likely that the lack of neurocognitive footing in clinical neuroimaging studies does not help for distinguishing the neural mechanisms that rely on DA neurotransmission<\/a> from those that rely on other systems. We especially think about the noradrenergic system, which might be involved in the functioning of BG-thalamo-cortical loops and executive functions (Albares et al., 2015b; Chamberlain et al., 2009; Faggiani and Benazzouz, 2017; Spay et al., 2018), but also about the serotoninergic (Carli and Invernizzi, 2014; Miguelez et al., 2014) and the cholinergic (Bohnen and Albin, 2011) systems.<\/p>\n https:\/\/neurotoolkit.com\/updrs\/<\/a><\/p>\n Criaud and collaborators (2016b) proposed that\u00a0 <\/span>akinesia …, an executive function which supports the gating of movement triggering to avoid inappropriate or premature responses in runcertain context (Jahanshahi et al., 2015a; 2015b). According to this view, akinesia could be considered as a de-automation symptom resulting partly from an impairment of the ability to switch from controlled to automatic action (Albares et al., 2015b; Favre et al., 2013; Hikosaka and Isoda, 2010; Isoda and Hikosaka, 2007; Jahanshahi et al., 1995; Jahanshahi et al., 2015a; 2015b; Siegert et al., 2002)<\/p>\n Restoration and targeting of aberrant neurotransmitters in Parkinson’s disease therapeutics<\/p>\n https:\/\/www.sciencedirect.com\/science\/article\/abs\/pii\/S0197018622000523<\/a><\/p>\n https:\/\/en.m.wikipedia.org\/wiki\/Abulia<\/a><\/p>\n \u00a0\u00a0<\/span><\/p>\n \u00a0<\/span><\/p>\n Parkinson Disease Can Be Viewed in Part as a Failure to Select Sensorimotor Options<\/i><\/b>\u00a0<\/span><\/b><\/b><\/p>\n The cardinal symptoms of Parkinson disease are akinesia (difficulties in initiating movement), bradykinesia (initiated movements are slow), and rigidity (stiffness and resistance to passive movement). Tremor is often but not always present. The principal neurological deficit responsible for the motor symptoms of Parkinson disease is thought to be the progressive degeneration of dopaminergic neurotransmission in the basal ganglia.<\/p>\n \u00a0<\/span>A consequence of this loss of dopamine is increased tonic and oscillatory activity in the recordings from basal ganglia output nuclei. Since the output of the basal ganglia is GABAergic and inhibitory, in Parkinson disease, targeted structures are receiving high and uneven levels of inhibitory input. This condition impairs the normal selective (disinhibitory) function of the basal ganglia; movements are difficult to select and, when possible, are slow to execute.\u00a0<\/span><\/p>\n Parkinson disease is, however, more nuanced than this. Over much of this progressive condition, the loss of dopaminergic transmission differentially affects the sensorimotor territories of the basal ganglia, leaving the limbic and associative territories comparatively unaffected. As discussed in the section on goal-directed and habitual control, the sensorimotor territories of the basal ganglia play an essential role in selecting habitual actions. Perhaps, therefore, it is not surprising that many of the motor features of Parkinson disease can be interpreted in terms of a loss of automatic habits. While patients can do things, they are trapped in the slower, serial, and voluntary mode of goal-directed control.<\/p>\n \u00a0\u00a0<\/span><\/p>\n \u00a0\u00a0<\/span><\/p>\n FoG and Freezing<\/p>\n FoG in PD overload<\/p>\n https:\/\/journals.plos.org\/plosone\/article?id=10.1371\/journal.pone.0144986#sec020<\/a> \u00a0<\/span><\/p>\n Subtypes<\/p>\n https:\/\/jamanetwork.com\/journals\/jamaneurology\/article-abstract\/1827554<\/a><\/p>\n Goal directed vs habitual control in the BG<\/p>\n https:\/\/pubmed.ncbi.nlm.nih.gov\/20944662\/<\/a><\/p>\n https:\/\/en.m.wikipedia.org\/wiki\/u<\/a><\/p>\n It is clear that other neurotransmitters<\/a> than DA play a role in the pathophysiology of PD (Bohnen et al., 2018; Braak et al., 2004; Delaville et al., 2012; Faggiani and Benazzouz, 2017; Fornai et al., 2007; Pahapill and Lozano, 2000; Politis et al., 2014). Yet, non-DA therapeutic strategies are still difficult to develop (Fox, 2013; Freitas and Fox, 2016). It is likely that the lack of neurocognitive footing in clinical neuroimaging studies does not help for distinguishing the neural mechanisms that rely on DA neurotransmission<\/a> from those that rely on other systems. We especially think about the noradrenergic system, which might be involved in the functioning of BG-thalamo-cortical loops and executive functions (Albares et al., 2015b; Chamberlain et al., 2009; Faggiani and Benazzouz, 2017; Spay et al., 2018), but also about the serotoninergic (Carli and Invernizzi, 2014; Miguelez et al., 2014) and the cholinergic (Bohnen and Albin, 2011) systems.<\/p>\n https:\/\/neurotoolkit.com\/updrs\/<\/a><\/p>\n Criaud and collaborators (2016b) proposed that\u00a0 <\/span>akinesia …, an executive function which supports the gating of movement triggering to avoid inappropriate or premature responses in runcertain context (Jahanshahi et al., 2015a; 2015b). According to this view, akinesia could be considered as a de-automation symptom resulting partly from an impairment of the ability to switch from controlled to automatic action (Albares et al., 2015b; Favre et al., 2013; Hikosaka and Isoda, 2010; Isoda and Hikosaka, 2007; Jahanshahi et al., 1995; Jahanshahi et al., 2015a; 2015b; Siegert et al., 2002)<\/p>\n Restoration and targeting of aberrant neurotransmitters in Parkinson’s disease therapeutics<\/p>\n https:\/\/www.sciencedirect.com\/science\/article\/abs\/pii\/S0197018622000523<\/a><\/p>\n