These results suggest that a past strong exposure to hazardous chemicals activates the PFC during olfactory stimuli in patients with MCS, and a strong activation in the OFC remains after the stimuli.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4434236/
Lack of contralateral suppression in transient-evoked otoacoustic emissions in multiple chemical sensitivity: a clinical correlation study.
Multiple chemical sensitivity (MCS) is a chronic disorder characterized by a variety of symptoms associated with the exposure to chemicals at a concentration below the toxic level. Previous studies have demonstrated peculiar responses in brain activity in these patients with respect to sensory stimuli while the association between chemical sensitivity and other environmental intolerances such as noise sensitivity has been questioned by researchers. In this study, a cohort of 18 MCS patients underwent transient-evoked otoacoustic emission (TEOAE) testing with and without contralateral suppression to evaluate the functionality of the medial olivocochlear (MOC) reflex involved in speech-in-noise sensitivity. Results were compared with an age- and gender-matched control group (n = 20) and correlation analysis with disease onset and quick environmental exposure sensitivity inventory (qEESI) symptom severity scale was performed. Subjects affected by MCS showed statistically significant impairment of MOC reflex, and the onset of the disease and several symptom subscales showed to be correlated to such reduction in some of the frequencies tested. These data suggest that alterations of MOC reflex could be part of the complex features of this disease although more studies are needed to further explore auditory perception disorders in environmental intolerances.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918670/
1.Symptoms are present for at least 6 months;
2.Symptoms occur in response to exposure to at least two of 11 common volatile chemicals;
3.Co-occurrence of at least one symptom from the CNS and one symptom from another organ system;
4.Symptoms cause significant lifestyle changes,
5.Symptoms occur when exposed and lessen or resolve when the symptom-triggering agent is removed;
6.Symptoms triggered by exposure levels do not induce symptoms in other individuals who are exposed to the same levels.
Neuropsychological and neuroimaging studies have shown––with a certain degree of debate — Several peculiar features in people affected by MCS and related illnesses. In particular, the prevalence of multiple personality traits as well as CNS hypereactivity and limbic kindling as key nodes in pathophysiological underpinnings of MCS was demonstrated.[21,22] In particular, the onset of MCS has been related to exposure to a “trigger” stimulus that alters CNS response in a way that subsequent stimuli are perceived as excessive and cause symptoms.[22]
Moreover, the relative hyperactivation found in some primary subcortical sensory structures (i.e., amygdala) — not counterbalanced by the same HC cortical activity and the same ability in controlling the arousing stimuli — was interpreted as neural behavioral changes related to low-level chemical exposures before emerging at the mind level.[5,23]
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4434236/
Lack of contralateral suppression in transient-evoked otoacoustic emissions in multiple chemical sensitivity: a clinical correlation study.
Multiple chemical sensitivity (MCS) is a chronic disorder characterized by a variety of symptoms associated with the exposure to chemicals at a concentration below the toxic level. Previous studies have demonstrated peculiar responses in brain activity in these patients with respect to sensory stimuli while the association between chemical sensitivity and other environmental intolerances such as noise sensitivity has been questioned by researchers. In this study, a cohort of 18 MCS patients underwent transient-evoked otoacoustic emission (TEOAE) testing with and without contralateral suppression to evaluate the functionality of the medial olivocochlear (MOC) reflex involved in speech-in-noise sensitivity. Results were compared with an age- and gender-matched control group (n = 20) and correlation analysis with disease onset and quick environmental exposure sensitivity inventory (qEESI) symptom severity scale was performed. Subjects affected by MCS showed statistically significant impairment of MOC reflex, and the onset of the disease and several symptom subscales showed to be correlated to such reduction in some of the frequencies tested. These data suggest that alterations of MOC reflex could be part of the complex features of this disease although more studies are needed to further explore auditory perception disorders in environmental intolerances.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918670/
1.Symptoms are present for at least 6 months;
2.Symptoms occur in response to exposure to at least two of 11 common volatile chemicals;
3.Co-occurrence of at least one symptom from the CNS and one symptom from another organ system;
4.Symptoms cause significant lifestyle changes,
5.Symptoms occur when exposed and lessen or resolve when the symptom-triggering agent is removed;
6.Symptoms triggered by exposure levels do not induce symptoms in other individuals who are exposed to the same levels.
Neuropsychological and neuroimaging studies have shown––with a certain degree of debate — Several peculiar features in people affected by MCS and related illnesses. In particular, the prevalence of multiple personality traits as well as CNS hypereactivity and limbic kindling as key nodes in pathophysiological underpinnings of MCS was demonstrated.[21,22] In particular, the onset of MCS has been related to exposure to a “trigger” stimulus that alters CNS response in a way that subsequent stimuli are perceived as excessive and cause symptoms.[22]
Moreover, the relative hyperactivation found in some primary subcortical sensory structures (i.e., amygdala) — not counterbalanced by the same HC cortical activity and the same ability in controlling the arousing stimuli — was interpreted as neural behavioral changes related to low-level chemical exposures before emerging at the mind level.[5,23]