Auditory brain-stem, middle- and long-latency evoked potentials in mild cognitive impairment

Irimajiri, Rie; Golob, Edward J.; Starr, Arnold

doi:10.1016/j.clinph.2005.04.010

Cited by 71 publications

(67 citation statements)

References 64 publications

(72 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…P 50 was reported to be diminished and prolonged or absent in Parkinson's disease, improving following posterior ansapallidotomy, except in one patient who showed mild worsening attributed to post-operative sleepiness (Mohamed et al, 1996). Increased P 50 amplitudes in mild cognitive impairment identified individuals who will subsequently convert to dementia (Irimajiri et al, 2005;Golob et al, 2007). Similar relationships have been identified in HIV-1 infection, correlating with indices of disease progression (Schroeder et al, 1994).…”

Section: Earlier Studies On P 50supporting

confidence: 54%

The auditory P50 component to onset and offset of sound

Pratt

Starr

Michalewski

et al. 2008

Clinical Neurophysiology

View full text Add to dashboard Cite

Objective: The auditory Event-Related Potentials (ERP) of component P 50 to sound onset and offset have been reported to be similar, but their magnetic homologue has been reported absent to sound offset. We compared the spatio-temporal distribution of cortical activity during P 50 to sound onset and offset, without confounds of spectral change. Methods: ERPs were recorded in response to onsets and offsets of silent intervals of 0.5 s (gaps) appearing randomly in otherwise continuous white noise and compared to ERPs to randomly distributed click pairs with half second separation presented in silence. Subjects were awake and distracted from the stimuli by reading a complicated text. Measures of P 50 included peak latency and amplitude, as well as source current density estimates to the clicks and sound onsets and offsets. Results: P 50 occurred in response to noise onsets and to clicks, while to noise offset it was absent. Latency of P 50 was similar to noise onset (56 ms) and to clicks (53 ms). Sources of P 50 to noise onsets and clicks included bilateral superior parietal areas. In contrast, noise offsets activated left inferior temporal and occipital areas at the time of P 50 . Source current density was significantly higher to noise onset than offset in the vicinity of the temporo-parietal junction. Conclusions: P 50 to sound offset is absent compared to the distinct P 50 to sound onset and to clicks, at different intracranial sources. P 50 to stimulus onset and to clicks appears to reflect preattentive arousal by a new sound in the scene. Sound offset does not involve a new sound and hence the absent P 50 . Significance: Stimulus onset activates distinct early cortical processes that are absent to offset.

show abstract

Section: Earlier Studies On P 50supporting

confidence: 54%

The auditory P50 component to onset and offset of sound

Pratt

Starr

Michalewski

et al. 2008

Clinical Neurophysiology

View full text Add to dashboard Cite

show abstract

“…The enhanced responses of somatosensory cortex are present early in the course of MCI (single domain) whereas the auditory cortical response is not affected until MCI becomes multiple domain and is independent of stimulus rate. Moreover, treatment with ChEI is without effect on the enhancement of auditory cortical activity (Irimajiri et al, 2005).…”

Section: Somatosensory Potentials In Mild Cognitive Impairment and Chmentioning

confidence: 96%

“…Specifically, both auditory and somatosensory but not visual sensory cortical activity appear to be enhanced in amplitude in subjects with MCI who are at high risk for developing dementia (Petersen et al, 1999). The enhancement of the somatosensory but not the auditory cortical activity in MCI is sensitive to modulation by ChEIs (Irimajiri et al, 2005). A longitudinal study of amnestic MCI subjects (Golob et al, in press) show that the amplitude increase of auditory P50 component differs between diagnostic subtypes of MCI, being evident in multiple-domain but not in single-domain MCIs.…”

Section: Clinical Implicationmentioning

confidence: 99%

See 1 more Smart Citation

Cholinesterase inhibitors affect brain potentials in amnestic mild cognitive impairment

et al. 2007

View full text Add to dashboard Cite

Amnestic mild cognitive impairment (MCI) is an isolated episodic memory disorder that hasa high likelihood of progressing to Alzheimer's disease. Auditory sensory cortical responses (P50, N100) have been shown to be increased in amplitude in MCI compared to older controls. We tested whether (1) cortical potentials to other sensory modalities (somatosensory and visual) were also affected in MCI and (2) cholinesterase inhibitors (ChEIs), one of the therapies used in this disorder, modulated sensory cortical potentials in MCI. Somatosensory cortical potentials to median nerve stimulation and visual cortical potentials to reversing checkerboard stimulation were recorded from 15 older controls and 15 amnestic MCI subjects (single domain). Results were analyzed as a function of diagnosis (Control, MCI) and ChEIs treatment (Treated MCI, Untreated MCI). Somatosensory and visual potentials did not differ significantly in amplitude in MCI subjects compared to controls.When ChEIs use was considered, somatosensory potentials (N20, P50) but not visual potentials (N70, P100, N150) were of larger amplitude in untreated MCI subjects compared to treated MCI subjects. Three individual MCI subjects showed increased N20 amplitude while off ChEIs compared to while on ChEIs. An enhancement of N20 somatosensory cortical activity occurs in amnestic single-domain MCI and is sensitive to modulation by ChEIs. IntroductionMild cognitive impairment (MCI) describes older individuals having cognitive impairments without accompanying functional impairments that characterize dementia (Petersen et al., 1999). Recent studies have suggested criteria for distinguishing among four subtypes of MCI based on the presence of both episodic memory impairment (amnestic or non-amnestic MCI) and other cognitive impairments (single-or multipledomain MCI) (Petersen, 2004). For example, amnestic singledomain MCI refers to patients with involvement of only memory deficit whereas amnestic multiple-domain MCI refers to patients with impairment of both memory and other cognitive domains such as language or executive function. MCI subjects have a high risk of converting to Alzheimer's disease Petersen et al., 1999) and show neuropathological features of β-amyloid plaques and neurofibrillary tangles similar to early Alzheimer's disease (Kordower et al., 2001;Mufson et al., 1999). These findings suggest that MCI can be a precursor of Alzheimer's disease. Cholinergic processes in neocortical areas are affected in Alzheimer's disease (Geula and Mesulam, 1989;Heckers et al., 1992) and are particularly apparent late in the course of

show abstract

“…We considered this hypothesis because P50 amplitude increases with normal aging and shows further increases in amnestic mild cognitive impairment that often anticipate the development of AD (Irimajiri et al, 2005;Golob et al, 2007). Amnestic mild cognitive impairment subjects that subsequently converted to AD had significantly larger P50 amplitudes than amnestic mild cognitive impairment subjects who remained stable (Golob et al, 2007).…”

Section: Auditory Cortical Sensory Potentialmentioning

confidence: 99%

ApoE genotype and abnormal auditory cortical potentials in healthy older females

Irimajiri

Golob

Starr

2010

Neurobiology of Aging

View full text Add to dashboard Cite

Apolipoprotein E (ApoE) status and gender are risk factors for the development of Alzheimer's disease. Alzheimer's disease is more prevalent in female relative to male carriers of the ApoE 4 gene. We examined cortical sensory (P50, N100) and cognitive (P300) potentials in an auditory target detection task in females as a function of ApoE genotype (ApoE 4 carriers, ApoE 4 non-carriers) to define the incidence of abnormalities prior to the clinical expression of cognitive impairments. Both neuropsychological test scores and sensory cortical potentials did not differ between the two ApoE groups. In contrast, cognitive P300 potentials were significantly decreased in amplitude and delayed in latency for ApoE 4 carriers compared to non-carriers. Four out of the 10 ApoE 4 carriers had abnormally (>2S.D.) delayed P300 latency compared to one out of 20 non-carriers. Abnormal cognitive processes reflected by P300 latency delays are expressed at significantly higher incidence in normal older females who are carriers of the 4 allele than in non-carriers of this allele.

show abstract

Auditory brain-stem, middle- and long-latency evoked potentials in mild cognitive impairment

Cited by 71 publications

References 64 publications

The auditory P50 component to onset and offset of sound

The auditory P50 component to onset and offset of sound

Cholinesterase inhibitors affect brain potentials in amnestic mild cognitive impairment

ApoE genotype and abnormal auditory cortical potentials in healthy older females

Contact Info

Product

Resources

About