Abstract
There is a growing interest in deep brain stimulation (DBS) of the nucleus basalis of Meynert (NBM) as a potential therapeutic modality for Parkinson’s disease dementia (PDD). Low-frequency stimulation has yielded encouraging results in individual patients; however, these are not yet sustained in larger studies. With the aim to expand the understanding of NBM-DBS, we share our experience with serendipitous NBM-DBS in patients treated with DBS of the internal Globus pallidus (GPi) for Parkinson’s disease. Since NBM is anatomically located ventral to GPi, several GPi-treated patients appeared to have the distal contact of DBS-electrode(s) positioned in the NBM. We hypothesized that unintentional high-frequency NBM-DBS over a period of one year would result in the opposite effect of low-frequency NBM-stimulation and cause cognitive decline. We studied a cohort of 33 patients with bilateral high-frequency DBS in the GPi for Parkinson’s disease, of which twelve were unintentionally co-stimulated in NBM. The subgroups of unintentional unilateral (N = 7) and bilateral NBM-DBS (N = 5) were compared to the control group of bilateral GPi-DBS (N = 11). Here, we show that unintentional high-frequency NBM-DBS did not cause a significantly faster decline in cognitive function. Further research is warranted for characterizing the therapeutic role of NBM-DBS.
Highlights
Parkinson’s disease (PD) is the fastest growing neurological disorder in the world [1]
Deep brain stimulation (DBS) as treatment for cognitive decline in Parkinson’s disease dementia (PDD) is a subject of ongoing interest [5]
nucleus basalis of Meynert (NBM) holds a pivotal role in a range of cognitive functions, including those commonly affected in PDD [7]
Summary
Parkinson’s disease (PD) is the fastest growing neurological disorder in the world [1]. A promising target is the nucleus basalis of Meynert (NBM) due to its widespread cholinergic innervation of the cortex (for a review of the NBM functional anatomy and evidence for involvement in the cognitive decline in PDD, see Gratwicke et al, 2013) [6]. NBM holds a pivotal role in a range of cognitive functions, including those commonly affected in PDD (arousal, attention, perception, and memory) [7]. This is in line with the tight correlation observed between the extent of NBM degeneration and cortical cholinergic deficits and cognitive decline [8]. Evidence regarding its clinical significance, has been equivocal (Table 1)
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