Objective: Investigate mismatch negativity in Parkinson disease with dementia.

Background: Parkinson’s disease with dementia (PDD) is an important cause of cognitive impairment in Parkinson’s disease and results in a major functional disability apart from motor deficits. It is a distinctive dementia, which characterized as impaired executive function, apathy, vivid hallucination and Lewy body pathology. There are many challenges in the field of dementia care. Treatment is very limited and purely symptomatic effect. However, to test new treatments effectively, one must be able to make early accurate diagnosis and has a biomarker that is sensitive and subjective to changes in disease severity. Mismatch negativity (MMN) is an EEG recorded electrophysiological signal reflecting the ability of novel signal detection by the brain. NMDA antagonist could ameliorate this event related potential. Here, we tried to developing a NMDA receptor dysregulation-related electrophysiology for the monitoring of clinical condition in PDD.

Methods: We recruited 7 PD patients and 15 PDD patients in our study. We tested the patients with auditory MMN while the difference in frequency were 1000 and 2000Hz. Standard stimuli was 80%. The interval between stimulation was 500 ms and a total of 500 trials were collected with a 32-channel EEG (ANT Mylab) with online reference of A1+A2. The pre-processing of the data was set as 500ms-epoch and eye-blink artefacts were rejected by 100μV . We measured mean amplitudes and peak latency between 150-250 ms from Fz electrode for further Student’s t test.

Results: We collected PD (65.4±7.3 y/o, F/M=4/3) and PDD patients (75.4±6.4 y/o, F/M=8/7). The averaged MMSE in PDD was 21.9. In the protocol 1000-2000 Hz, the Peak amplitude of PDD was significantly smaller than PD patients (PD:-3.8±2.0μV, PDD:-2.2±1.9μV; p=0.01). On the other hand, the peak latencies of MMN between PD and PDD patients have no significant difference (PD: 161±14 ms, PDD: 163±15 ms; p=0.67).

Conclusions: We found reduced MMN amplitudes in Parkinson disease dementia patients in comparison with PD patients. This result may link to abnormal NMDA related plasticity change in cortical level in PDD. The widespread Lewy body pathology in cortical level may be the explanation to this finding. We may further collect the patients and utilize this result as a possible biomarker in the detection of disease progression in Parkinson dementia patients.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/abnormal-nmda-related-electrophysiology-in-parkinson-disease-dementia/