title: Structural brain abnormalities in patients with inflammatory illness acquired following exposure to water-damaged buildings: a volumetric MRI study using NeuroQuant®.
abstract: Executive cognitive and neurologic abnormalities are commonly seen in patients with a chronic inflammatory response syndrome (CIRS) acquired following exposure to the interior environment of water-damaged buildings (WDB), but a clear delineation of the physiologic or structural basis for these abnormalities has not been defined. Symptoms of affected patients routinely include headache, difficulty with recent memory, concentration, word finding, numbness, tingling, metallic taste and vertigo. Additionally, persistent proteomic abnormalities in inflammatory parameters that can alter permeability of the blood-brain barrier, such as C4a, TGFB1, MMP9 and VEGF, are notably present in cases of CIRS-WDB compared to controls, suggesting a consequent inflammatory injury to the central nervous system. Findings of gliotic areas in MRI scans in over 45% of CIRS-WDB cases compared to 5% of controls, as well as elevated lactate and depressed ratios of glutamate to glutamine, are regularly seen in MR spectroscopy of cases. This study used the volumetric software program NeuroQuant® (NQ) to determine specific brain structure volumes in consecutive patients (N=17) seen in a medical clinic specializing in inflammatory illness. Each of these patients presented for evaluation of an illness thought to be associated with exposure to WDB, and received an MRI that was evaluated by NQ. When compared to those of a medical control group (N=18), statistically significant differences in brain structure proportions were seen for patients in both hemispheres of two of the eleven brain regions analyzed; atrophy of the caudate nucleus and enlargement of the pallidum. In addition, the left amygdala and right forebrain were also enlarged. These volumetric abnormalities, in conjunction with concurrent abnormalities in inflammatory markers, suggest a model for structural brain injury in "mold illness" based on increased permeability of the blood-brain barrier due to chronic, systemic inflammation.
authors.affiliation: Center for Research on Biotoxin Associated Illnesses, Pocomoke, MD, United States. Electronic address: ritchieshoemaker@msn.com.
authors.forename: Ritchie C
authors.initials: RC
authors.lastname: Shoemaker
authors.affiliation: Center for Research on Biotoxin Associated Illnesses, Pocomoke, MD, United States.
authors.forename: Dennis
authors.initials: D
authors.lastname: House
authors.affiliation: Proteogenomics, Vero Beach, FL, United States.
authors.forename: James C
authors.initials: JC
authors.lastname: Ryan
mesh_terms: D000328:Adult; D001921:Brain / Q000473:pathology*; D001330:Electronic Data Processing; D004660:Encephalitis / Q000473:pathology*; D004781:Environmental Exposure / Q000009:adverse effects*; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D014867:Water / Q000009:adverse effects; D055815:Young Adult
chemical_list: D014867:Water
keywords: Blood–brain barrier; Caudate nucleus; Microscopic interstitial edema; NeuroQuant; TGF beta-1; Volumetric MRI