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Attention and bradyphrenia

In 1922, the neurologist F. Naville introduced the concept of bradyphrenia, a condition characterized by slow cognition, apathy, and impaired concentration [40]. The term originated in the context of an epidemic of encephalitis lethargica in the 1920s which resulted in parkinsonism and the psychiatric syndrome that became to be known as bradyphrenia. The term ‘bradyphrenia’ is frequently used in the older literature on cognitive deficits in PD. However, even initially there were conflicting results regarding the relationship between parkinsonism and bradyphrenia. In 1924, Worster-Drought and Hardcastle found that reduced psychomotor speed, but not an increase in ‘cerebration time’ (‘thinking time’), was associated with parkinsonism [40]. Authors such as Mayeux have suggested that slowed cognition is a cause of, or at least closely related to, deficits of alertness in PD [41].

In PD-D, there is consistent ERP-based evidence of slowed cognition. In a study investigating both auditory and visual ERPs in HC, PD-D, AD, and PD, auditory P300 and flash visual-evoked potential latency measures were significantly increased in the PD-D group compared with controls [42]. Increased ERP-latencies in PD-D have also been found in other studies [43]. Two studies have directly compared P300 latency in both PD-D and PD relative to HC. In both studies P300 latencies were normal in the PD groups but increased in the PD-D groups [44, 45].

Pate and Margolin [46], who used two reaction time tasks, concluded that motor, as well cognitive, slowing was present in both PD and PD-D, and that such slowing was disproportionate to the level of general cognitive impairment compared with a group of AD patients. However, Goldman et al. [47] compared 22 patients with mild PD-D with 58 non-impaired PD patients and 48 HC. They found slow movement time, but no increase in cognitive reaction time in either PD or mild PD-D. Nevertheless, the study of Ballard et al. [25] showed that cognitive reaction time was slower in PD-D than in PD and AD, being comparable to that in DLB. The PD patients without dementia had slower choice reaction time than the HC but a similar variability of reaction time. Thus, this study indicates that slow cognition is associated with cognitive decline in PD, and its severity is disproportionately large in PD-D and DLB compared with AD.

The concept of bradyphrenia and ‘slow cognition’ may be problematic in relation to the attention construct and also to other cognitive functions. The study by Mayeux et al. [41] illustrates the problem. Poor performance on a vigilance task was deemed to be due to ‘bradyphrenia’. What then is the relationship between ‘bradyphrenia’ and ‘vigilance’ or ‘alertness’? A solution is offered in Timothy Salthouses [48] processing speed theory of adult age differences in cognition. Salthouse proposes that slowed cognition (bradyphrenia) is a general mechanism underlying the age-related decline in cognitive performance. The assumption is that any complex mental task is executed by multiple cognitive component processes with associated neural underpinnings. If one or more of these processes runs more slowly because of pathology affecting the associated neural substrate(s), the mental task will either be solved more slowly or not solved successfully at all (if it depends on a timing restraint). This is the case in perceptual detection tasks, where the presentation of external stimuli cannot be slowed down by the perceiver. In this case, slowed cognition may, for instance, lead to missed target stimuli. Salthouse calls this phenomenon a ‘limited time’ mechanism. Slow component cognitive processes can also lead to deficits when the product of early processing stages is no longer available for use in a later processing stage. Salthouse calls this the ‘simultaneity mechanism’ [48]. The latter may, for instance, be the case in working memory tasks where cognitive manipulation of working memory content is dependent upon active maintenance of this content. Thus, slow cognition and deficits in vigilance/alertness are phenomena on different analytical levels. Slow cognition is a neural and mental mechanism, while vigilance/ alertness deficits are behavioural manifestations of this mechanism. The evidence overall indicates that not all PD patients experience cognitive slowing, but that cognitive slowing is associated with cognitive decline and dementia and that it may be closely related to the aetiology of the cognitive decline in PD to a larger degree than in AD.

In summary, the combined evidence shows that executive and attentional dysfunctions are cognitive hallmarks of PD-D compared with AD. When compared with DLB, the deficits overall appear to be somewhat less severe. However, the studies that have compared ‘fluctuations’, defined as variability of reaction time [25, 31], both showed that fluctuating attention was at least as severe in PD-D as in DLB.

 
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