Table 2: Summary of theories of cognition and the clinical implications.
Theory |
Summary |
Clinical Implications
|
The Braak Model Braak, et al. (2003) |
· PD progresses in a caudal-rostral fashion via 6 stages. · Stages 1-2: Pathology initiates in peripheral regions. Patients are initially asymptomatic. Autonomic dysfunction present by stage 2. · Stages 3-4: Pathology progresses to the subcortex. Symptoms include disturbed sleep, tremor, rigidity, and slowness of movement. MCI may arise due to disrupted neural connectivity. · Stages 5-6: Pathology progresses to the cortex. Symptoms include cognitive impairment, possibly dementia. |
· Non-motor symptoms (e.g., sleep, decreased olfaction) regulated by peripheral regions appear early in the disease, often before the traditional motor symptoms. · Younger patients who have a longer clinical course tend to have pathology that fits with Braak’s model of progression, compared to those with older onset and shorter disease duration. · Clinicians should continually assess non-motor symptoms as they often present in a dynamic manner. |
The GO/NoGo Model Frank (2006) Frank, et al. (2004) |
· The direct and indirect basal ganglia pathways interact to facilitate desired actions and inhibit undesired actions. · Alterations in dopamine levels either enhance or impede functioning of the direct and indirect pathways. · The effectiveness of positive versus negative feedback varies depending on dopaminergic medication status. |
· Errorless learning approaches may be particularly useful with individuals with PD given impaired trial-and-error learning capabilities. · Medication status may influence the effectiveness of reinforcement during therapy, with negative reinforcement more effective off medication and positive reinforcement more effective on medication. · Some individuals with PD are particularly susceptible to pathological gambling and addiction with dopamine supplementation. |
The Dopamine-Overdose Hypothesis Cools, et al. (2001) Swainson, et al. (2000)
|
· Dopaminergic medication will “refill” the dorsal striatum and enhance the associated cognitive functions (e.g., set-shifting), but can “overdose” the ventral striatum and degrade associated cognitive functions (e.g., reward performance, impulsivity). |
· Improvement in the motor functions of PD can come at the expense of cognitive functions. · Variability in treatment outcomes for cognitive goals may be driven by medication status. · Motor sequence learning, important for instrumental activities of daily living such as technology use and driving, can become impaired by medication in early PD. |
The Neural Networks Framework Gratwicke, et al. (2015) |
· Cognitive functions are influenced by overlapping neural networks. Degradation of these networks can lead to MCI or dementia. · Executive dysfunction in PD results from dopamine depletion in the striatum and subsequent interruption of fronto-striatal networks. · Impairments in attention, memory, and visuospatial perception may be attributed to degenerating cholinergic and noradrenergic pathways. |
· Patients prescribed noradrenergic or cholinergic medications may have more advanced cognitive decline. The presence of these medications should cue clinicians to conduct thorough cognitive evaluations. |
The Dual-Syndrome Hypothesis Kehagia, et al. (2013) |
· There are two primary cognitive phenotypes in PD. · Dysexecutive syndrome: Primary deficits in working memory and executive functions, is mediated by fronto-striatal pathways, and is affected by dopaminergic medication. · Dementia syndrome: Early-presenting deficits of visuospatial function and semantic fluency that are mediated by posterior-cortical regions, and not affected by dopaminergic medication. Impairments may be amenable to cholinergic medications. |
· Early deficits in visuospatial skills and semantic fluency are associated with progression to dementia. · Individuals may present with variable performance on cognitive tasks related to the dysexecutive syndrome once beginning medication. |