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Titolo:
WHITE PAPER - NEUROPSYCHIATRIC ASPECTS OF SENSITIVITY TO LOW-LEVEL CHEMICALS - A NEURAL SENSITIZATION MODEL
Autore:
BELL IR;
Indirizzi:
TUCSON VET AFFAIRS MED CTR,3601 S 6TH AVE,MS 116A TUCSON AZ 85723 UNIV ARIZONA,HLTH SCI CTR,DEPT PSYCHIAT TUCSON AZ 00000
Titolo Testata:
Toxicology and industrial health
fascicolo: 4-5, volume: 10, anno: 1994,
pagine: 277 - 312
SICI:
0748-2337(1994)10:4-5<277:WP-NAO>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
ORGANIC-SOLVENT EXPOSURE; POSTTRAUMATIC-STRESS-DISORDER; TIME-DEPENDENT SENSITIZATION; SELF-REPORTED ILLNESS; PITUITARY-ADRENAL AXIS; CENTRAL-NERVOUS-SYSTEM; BEHAVIORAL SENSITIZATION; RISK-FACTORS; ORGANOPHOSPHATE PESTICIDE; ENVIRONMENTAL ILLNESS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
143
Recensione:
Indirizzi per estratti:
Citazione:
I.R. Bell, "WHITE PAPER - NEUROPSYCHIATRIC ASPECTS OF SENSITIVITY TO LOW-LEVEL CHEMICALS - A NEURAL SENSITIZATION MODEL", Toxicology and industrial health, 10(4-5), 1994, pp. 277-312

Abstract

The present paper summarizes the proposed time-dependent sensitization (TDS) and partial limbic kindling model for illness from low-level chemicals; reviews and critiques prior studies on CNS aspects of multiple chemical sensitivity (MCS); and outlines possible experimental approaches to future studies. TDS is the progressive and persistent amplification of behavioral, neurochemical, endocrine, and/or immunological responses to repeated intermittent stimuli over time. Partial limbic kindling is a progressive and persistent lowering of the threshold for eliciting electrical afterdischarges, but not motor seizures, in certain brain structures such as amygdala and hippocampus; behavioral consequences include increased avoidant behaviors. The focus of the paper is the controversial claim of altered sense of smell and illness from low levels of environmental chemicals (i. e., ''cacosmia''), levels that should not have any biologically harmful effects by the rules of classical neurotoxicology. A major perspective of this paper is that the phenomenology of MCS is similar to that of time-dependent sensitization (reverse tolerance) and tolerance as studied in the substance abuse literature. The TDS model for MCS proposes that neurobiological amplification underlies the symptoms and phenomenology of these patients, including their behavioral features of heightened affective and somatic distress. It is hypothesized that MCS patients, who are mostly women, may be individuals who sensitize to substances rapidly and to the extreme, to the point of aversive symptomatology with less complete capacity far development of tolerance. Possible parallels between MCS and TDS include: (a) initiation by single or multiple intermittent stimuli; (b) lasting changes in subsequent reactivity to low levels of chemically unrelated substances; (c) cross-sensitization between the stressorsand pharmacological agents; (d) greater vulnerability of individuals who are female, who have certain genetic characteristics, and/or who may be hyperreactive to novelty (cf trait shyness); (e) lack of obviousdifferences between sensitized and unsensitized individuals at baseline without eliciting exposures; (f) bidirectionality (bipolarity) of sensitized responses; (g) both context-dependent (conditioned) and context-independent (unconditioned) amplification of responses. To minimize variability between studies, research in this area needs (a) consensus on a working case definition of MCS or at least of cacosmia as a specific symptom in a subset of well-defined medical and psychiatric disorders; and (b) proper design of chemical challenge studies in MCS, controlling for individual differences in sensitizability and for the properties of sensitization (e.g., repeated intermittent exposure tests)and tolerance (e.g., removal from customary ambient air exposures prior to testing). Several studies have shown that psychiatric histories in MCS include increased rates of major depression, panic and other anxiety disorders, and somatization disorder. Skeptics of MCS and cacosmia suggest that the problem is one of psychogenic symptom amplification and misattribution of psychiatric symptoms to chemicals; they dismiss MCS as the twentieth century version of ''hysteria (i.e., somatization disorder). '' However, no previous investigations of psychopathologyin MCS patients have reported systematic assessments, including chemical exposure challenge studies, to rule out organic factors in etiology. A number of investigators have previously proposed that TDS and/or partial limbic kindling offer a neurobehavioral model for the same psychiatric conditions found at increased rates in MCS. Furthermore, recent data suggest that psychological variables are a correlate of but not a full explanation for cacosmia. Medical histories reported by cacosmics include increased rates of physician-diagnosed irritable bowel, migraine headache, nasal allergies, hypothyroidism, and breast and ovarian cysts. Such medical histories suggest possible directions in the search for objective markers, such as functional studies of the hypothalamic-pituitary-adrenal system, endogenous opioid peptides, the thyroid axis, and breast and ovarian ultrasound combined with reproductive hormone patterns. ''Hysteria'' has no known causes or treatments in modern psychiatry. Systematic research on MCS may provide new, insights into old questions to facilitate advances in medicine, neuropsychiatry,and clinical neuroscience.

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Documento generato il 27/01/21 alle ore 01:45:11