Better living through brain chemistry?
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Positron emission tomography permits examination of the chemistry of the brain in living human beings. Until recently, positron emission tomography had been considered a research tool, but it is rapidly moving into clinical practice. This report describes the uses and applications of positron emission tomography in examinations of patients with strokes, epilepsy, malignancies, dementias, and schizophrenia and in basic studies of synaptic neurotransmission.
The neurobiology of the interaction between pain and anxiety is unknown. The present study examined interrelationships between: regional brain chemistry (as identified by in vivo proton magnetic resonance spectroscopy [(1)H-MRS] in dorsolateral prefrontal cortex [DLPFC], orbitofrontal cortex [OFC], cingulate and thalamus), pain (as measured by short form of the McGill Pain Questionnaire [SF-MPQ]), and anxiety (measured by the State-Trait Anxiety Inventory) in chronic low back pain (CLBP) patients, and contrasted to the relationship between brain chemistry and anxiety in sex and age-matched normal subjects. The results show that brain chemistry depends on a 3-way interaction of brain regions examined, subject groups (normal vs. CLBP), and anxiety levels (high vs. low). The concentration of N-Acetyl aspartate (the largest peak in (1)H-MRS) in OFC could distinguish between anxiety levels and between subject groups. Chemical-perceptual relationships were analyzed by calculating correlations between regional chemicals and perceptual measures of pain and anxiety. To isolate pain from anxiety, these maps were subdivided based on anxiety and, in the CLBP patients along anxiety-more-related vs. anxiety-less-related pain descriptors and along sensory vs. affective pain descriptors. There was a precise relationship between perception and brain chemistry. The chemical-perceptual network best related to pain in CLBP patients was comprised of the DLPFC and OFC; the chemical-anxiety network was best related to the OFC chemistry in normals and to all four regions studied in CLBP patients; and the cingulate was best related to the affective component of pain. We conclude that the chemical-perceptual mapping differentiates between closely related perceptual states of pain and anxiety in chronic pain and provides a brain regional-chemical-perceptual description of the long-term reorganization that occurs with chronic pain.
Glutamic acid and GABA concentrations were measured in brain areas of rats injected with the chloride salts of Li+, Na+, K", Rb+ or Cs+ for 5 days. Regional changes in brain glutamic acid and GABA were found in animals after lithium, rubidium or cesium, but not potassium, compared to sodium treatments. Increased glutamic acid and GABA levels, caused by lithium and rubidium, were found in brain structures (hypothalamus and amygdala) known to be involved in emotional behavior. Whether these changes are associated with the effective use of lithium and, perhaps, of rubidium in affective disorders remains obscure.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The neurobiology of chronic pain, including chronic back pain, is unknown. Structural imaging studies of the spine cannot explain all cases of chronic back pain. Functional brain imaging studies indicate that the brain activation patterns are different between chronic pain patients and normal subjects, and the thalamus, and prefrontal and cingulate cortices are involved in some types of chronic pain. Animal models of chronic pain suggest abnormal spinal cord chemistry. Does chronic pain cause brain chemistry changes? We examined brain chemistry changes in patients with chronic back pain using in vivo single- voxel proton magnetic resonance spectroscopy ((1)H-MRS). In vivo (1)H-MRS was used to measure relative concentrations of N-acetyl aspartate, creatine, choline, glutamate, glutamine, gamma-aminobutyric acid, inositol, glucose and lactate in relation to the concentration of creatine. These measurements were performed in six brain regions of nine chronic low back pain patients and 11 normal volunteers. All chronic back pain subjects underwent clinical evaluation and perceptual measures of pain and anxiety. We show that chronic back pain alters the human brain chemistry. Reductions of N-acetyl aspartate and glucose were demonstrated in the dorsolateral prefrontal cortex. Cingulate, sensorimotor, and other brain regions showed no chemical concentration differences. In chronic back pain, the interrelationship between chemicals within and across brain regions was abnormal, and there was a specific relationship between regional chemicals and perceptual measures of pain and anxiety. These findings provide direct evidence of abnormal brain chemistry in chronic back pain, which may be useful in diagnosis and future development of more effective pharmacological treatments.
Explore the source record for details and available documents.
Within the last two decades it has become evident that the brain exhibits a wide range of chemical and physiological responses to its sensory environment. Comparison of the brains of animals reared in relatively complex as opposed to deprived sensory environments has yielded significant insight into the nature of these effects, which are reviewed in this paper. Greater complexity of the sensory environment results in increased total cholinesterase and acetylcholinesterase enzyme activity, while other neurotransmitter related substances, the catecholamines, show more variable responses. RNA concentration is slightly greater as is DNA transcriptional activity, while protein precursor uptake shows a variety of regional and temporal patterns. In general, responses for most substances tend to show regional and temporal specificity with the largest effects most often in the occipital cortex. Electrophysiological measures have revealed shorter visual cortex evoked potential latencies and greater amounts of sleep in the complexity-reared subjects. The wide range of environmentally responsive parameters is consistent with an adaptive functioning of brain chemistry and physiology and with recent models in the physical sciences which view the universe as composed of dynamic webs of relationships rather than isolated independent units.
We studied brain temperature and the effect of mild hypothermia in 58 patients after severe head injury (SHI). Brain tissue oxygen tension (ptiO2), carbon dioxide tension (ptiCO2), tissuie pH (pHti) and temperature (T.br) were measured using a multiparameter probe. Microdialysis was performed to measure glucose, lactate, glutamate, and aspartate in the extracellular fluid. Mild hypothermia (34 degrees-36 degrees C) was employed in 33 selected patients who had persistent increased intracranial pressure (ICP > 20 mmHg). Mild induced hypothermia decreased brain oxygen significantly from 33 +/- 24 mmHg to 30 +/- 22 mmHg (p < 0.05). The ptiCO2 (46 +/- 8 mmHg) was also significantly lower during mild hypothermia (40.4 +/- 4.0 mmHg), p < 0.0001). The pHti increased from 7.13 +/- 0.15 to 7.24 +/- 0.10 (p < 0.0001) under hypothermic conditions. Induced hypothermia may protect patients from secondary ischemic events by lowering the critical ptiO2 threshold, reducing anaerobic metabolism, and decreasing the release of excitatory aminoacids. However, patients with spontaneous brain hypothermia on admission (Tbr < 36.0 degrees C) showed significantly higher levels of glutamate as well as lactate, compared to all other patients, and had a worse outcome. Spontaneous brain hypothermia carries a poor prognosis, and was characterized by markedly abnormal brain metabolic indices.
Explore the source record for details and available documents.
CONTEXT: The brain pathophysiological abnormalities underlying autism remain unclear. Neuroimaging and histological studies suggest cellular abnormalities early in the course of the disease. OBJECTIVE: To measure the in vivo chemical profile of gray and white matter tissues in autism. DESIGN: Cross-sectional spectroscopic imaging study comparing 3- to 4-year-old children with autism spectrum disorder (ASD) with age-matched comparison groups of children with delayed development (DD) and typical development (TD). SETTING: The University of Washington Diagnostic Imaging Sciences Center, Seattle. PARTICIPANTS: Forty-five 3- to 4-year-old children with ASD, 12 age-matched children with DD, and 10 age-matched children with TD. MAIN OUTCOME MEASURES: Estimates of gray and white matter concentrations for choline-containing compounds (Cho), creatine plus phosphocreatine, N-acetylaspartate (NAA), and myo-inositol (mI). Transverse relaxation times for Cho, creatine plus phosphocreatine, and NAA expressed relative to control subjects with TD were examined to evaluate tissue compactness. RESULTS: The children with ASD demonstrated decreased gray matter concentrations of Cho (P < .001), creatine plus phosphocreatine (P = .02), NAA (P = .02), and mI (P = .008) compared with children with TD. Gray matter Cho transverse relaxation was also prolonged for the ASD sample compared with the TD group (P = .01). The children with ASD demonstrated significantly decreased levels of Cho (P = .04) and mI (P = .008) and trend-level NAA (P = .09) in gray matter compared with the DD group. For white matter, both children with ASD and children with DD showed a similar pattern of NAA and mI level decreases (for children with ASD vs children with TD: NAA, P = .03; mI, P = .04; for children with DD vs children with TD, NAA, P = .03; mI, P = .07). In several analyses, cerebral volume contributed significantly as a covariate. CONCLUSIONS: Reduced gray matter chemical concentrations and altered Cho transverse relaxation, in a pattern distinct from that in children with DD, suggest decreased cellularity, or density, at this early time point in ASD. Possibly reflecting shared developmental features, white matter results were common to ASD and DD groups. The relationship between cerebral volume and neurochemistry at this early time point may indicate processes related to unit scaling.
BACKGROUND: Prior work reported elevated gray matter (GM) lactate and Glx (glutamate + glutamine + GABA) concentrations in unmedicated patients with bipolar disorder (BP) compared with healthy controls (HC). This study examined whether lithium (Li) and valproic acid (VPA) treatment modulated these chemicals. METHODS: A subset of previously reported BP patients were treated with Li (n = 12, 3.6 +/- 1.9 months) or VPA (n = 9, 1.4 +/- 1.7 months) and compared untreated HC subjects (n = 12, 2.9 +/- 2.4 months) using proton echo-planar spectroscopic imaging. Regression analyses (voxel gray/white composition by chemistry) were performed at each time point, and change scores computed. Metabolite relaxation and regions of interest (ROI) were also examined. RESULTS: Across treatment, Li-treated BP subjects demonstrated GM Glx decreases (Li-HC, p =.08; Li-VPA p =.04) and GM myo-inositol increases (Li-HC p =.07; Li-VPA p =.12). Other measures were not significant. Serum Li levels were positively correlated with Glx decreases at the trend level. CONCLUSIONS: Li treatment of BP was associated with specific GM Glx decreases and myo-inositol increases. Findings are discussed in the context of cellular mechanisms postulated to underlie Li and VPA therapeutic efficacy.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.