Neuroinflammation as secondary damage in head injury

Head injury is one of the main disability causes among the working-age population. Stroke energy induces mechanical injury of tissues to launch secondary damage, i.e. neurotransmission, blood-brain barrier disruption, blood infiltration of brain tissues, cytokine and chemokine overexpression, and other processes. Activated by the injury, microglia plays a special part to initially 'protect' intact tissues from the products of necrosis and apoptosis. After the injury, microglia rapidly differentiates to phenotypes М1 and М2. Pro-inflammatory phenotype М1 produces neuronal cytotoxic cytokines including tumor necrosis factor-, interleukins (IL)-6 and IL-1, and NO that induce apoptosis while phenotype М2 secretes IL-4 and IL-13 that may supposedly reduce inflammation and improve recovery of brain tissues. М2 response lasts much less than М1 response, and increasing pro-inflammatory activation leads to further neuronal death, which affects cognitive and physical status of patients with head injury. The review covers main biochemical processes in the injured brain and possible ways of neuroinflammation modulation

Frontal and temporal lobe sources from mismatch negativity (MMN) in schizophrenia: an ERP and MR anatomical imaging study

BACKGROUND: MMN is an electrophysiological measure of automatic auditory change detection. A smaller MMN in patients with schizophrenia1,2 may reflect altered frontal activity3. METHODS: Following our report on the coordinates for frontal and temporal lobe dipole-loci contributing to normal MMN4, we replicated this result using brain electrical source analysis (BESA) and MR-images of the brain in 14 healthy subjects (34.8 years) and compared it with 17 patients (32 years) 15 years after the onset of schizophrenia. RESULTS: For MMN associated with a frequency deviant tone, asymmetric loci in the superior-temporal and left anterior-cingulate gyri were replicated, while that in the right inferior-frontal gyrus moved to the mid-frontal border (residual variance [RV] < 1%). Patients showed a modest MMN reduction, a weaker left temporal lobe source but essentially similar loci (RVf1%). Discrete changes in the locus of left temporal and cingulate sources were illustrated by plotting volumes around the group solution for individual’s data to 2% RV, with the radius illustrating the standard deviation of the distance to the better solutions for other subjects’ loci (also using a 2% RV criterion). The left temporal lobe source was marginally more medial in patients (5 mm, p < 0.01), while the left cingulate was more rostral (10 mm, p < 0.0001). CONCLUSION: The data show a degree of compensation of function despite altered source locations in the left hemisphere

Frontal and temporal sources of mismatch negativity in healthy controls, patients at onset of schizophrenia in adolescence and others at 15 years after onset

Mismatch negativity (MMN) is an event-related potential measure of auditory change detection. It is widely reported to be smaller in patients with schizophrenia and may not improve along with otherwise successful clinical treatment. The main aim of this report is to explore ways of measuring and presenting four features of frequency-deviant MMN dipole sources (dipole moment, peak latency, brain location and orientation) and to relate these to the processes of psychopathology and illness progression. Data from early onset patients (EOS) at the start of the illness in adolescence, and others who had their first break in adolescence 15 years ago (S-15Y) were compared with two groups of age-matched healthy controls (C-EOS, C-15Y). A four-source model fitted the MMN waveform recorded from all four groups, whether MMN amplitude was more (EOS) or less (S-15Y) reduced. The locations were in the left superior temporal and anterior cingulate gyri, right superior temporal and inferior/mid frontal cortices. Dipole latencies confirmed a bottom-up sequence of processing and dipole moments were larger in the temporal lobes and on the left. Patients showed small dipole location changes that were more marked in the S-15Y than the EOS group (more rostral for the left anterior cingulate, more caudal for the right mid-frontal dipole) consistent with illness progression. The modelling of MMN dipole sources on brain atlas and anatomical images suggests that there is a degree of dissociation during illness between small progressive anatomical changes and some functional recovery indexed by scalp recordings from patients with an onset in adolescence 15 years before compared to adolescents in their first episode. © 2004 Elsevier B.V. All rights reserved.link_to_subscribed_fulltex