A combined study of tumor-related brain lesions using MEG and proton MR spectroscopic imaging.

The purpose of this study is to localize, in cases of brain tumors, pathological magnetic brain activities and to analyze metabolic alterations in functionally abnormal lesions using magnetoencephalography (MEG) and proton magnetic resonance spectroscopic imaging (1H MRSI). The study focused on 10 healthy volunteers and seven patients with common brain tumors, namely astrocytic tumor and meningioma. In spontaneous MEG, the pathological brain activities (slow, fast waves and spikes) were localized using a single equivalent dipole model. After the results of MEG and 1H MRSI were superimposed onto the corresponding MR images, the signal intensities of spectroscopically visible metabolites were analyzed in the regions where the dipoles of the pathological activities were concentrated. Increased slow wave activity was observed in four cases and fast wave or spike activity was significantly increased in one case. These pathological activities were localized in surrounding regions of the bulk of tumors, where mild reduction of N-acetyl aspartate (NAA) and slight accumulation of lactate (Lac) consistently existed. Preserved cortical areas, which are indicated by residual NAA, might be able to generate pathological magnetic activities under lactic acidosis. Such areas could be understood as a border zone between normal and seriously damaged brain tissue by tumors or associated brain edema. This combined technique with the different modalities gives insight into functional as well as metabolic aspects of pathological brain conditions.

A combined study of tumor-related brain lesions by using magnetoencephalography and 1H magnetic resonance spectroscopic imaging. Technical note.

The purpose of this study was to localize pathological magnetic brain activities and to analyze metabolic alterations in functionally abnormal lesions by using magnetoencephalography (MEG) and (1)H magnetic resonance (MR) spectroscopy in patients with brain tumors. The authors studied 10 healthy volunteers and seven patients who harbored common brain tumors, namely astrocytic tumors and meningioma. In spontaneous MEG the pathological brain activities (slow waves, fast waves, and spikes) were localized using a single equivalent dipole model. After the results of MEG and (1)H MR spectroscopy were superimposed onto the corresponding MR images, the signal intensities of spectroscopically visible metabolites were analyzed in the regions in which the dipoles of the pathological activities were concentrated. Increased slow-wave activity was observed in four cases, and fast-wave or spike activity was significantly increased in one case each, respectively. These pathological activities were localized at almost the same cortical areas adjacent to the bulk of tumors, where mild reduction of N-acetyl aspartate (NAA) and slight accumulation of lactate consistently existed. Preserved and metabolically active cortical areas, which are indicated by residual NAA, might be able to generate pathological magnetic activities under lactic acidosis. Such an area could be understood as a border zone between normal brain tissue and brain tissue that has been seriously damaged by tumors or associated edema, which should be intensively treated. This combination of imaging techniques gives insight into functional as well as metabolic aspects of pathological brain conditions.

Responses to silent Kanji reading of the native Japanese and German in task subtraction magnetoencephalography.

The neuromagnetic activities evoked by semantic processing were localized by magnetoencephalography (MEG). We observed distinct time courses of the activities in native speaking Japanese subjects (Japanese speaker) and German subjects (German speaker) during silent reading of Japanese letters; Kanji and meaningless figures made by deforming the Arabian letters. There were significant differences in amplitude of the activities between Kanji and meaningless figure stimuli. The responses with meaningless figure stimuli were subtracted from those with Kanji stimuli to demonstrate the semantic responses. Earlier responses peaked at about 273.3+/-50. 8 and 245.0+/-23.8 ms (mean+/-S.D.) and were mainly located in the right fusiform gyrus (FuG) in the Japanese and German speakers, respectively. All the Japanese speakers constantly showed additional later responses in the left superior temporal gyrus (STG) and the supramarginal gyrus (SmG) at approximately 616.1+/-105.5 ms, whereas no further activity was observed in the German speakers who did not know the meaning of each Kanji. Because the later responses in the STG and SmG in the Japanese speakers were only observed in their dominant hemisphere, we believe the source of these responses to be part of the neural basis of Kanji semantic processing. The task subtraction MEG analysis could be a powerful method to discriminate distinct responses and visualize the neural networks involved in semantic processing.

Localization analysis of neuronal activities in benign rolandic epilepsy using magnetoencephalography.

Benign epilepsy of childhood with rolandic spikes (BECRS) is an electroclinical syndrome characterized by partial sensorimotor seizures with centrotemporal spikes. We report a detailed localization analysis of spontaneous magnetic brain activities in seven BECRS patients using magnetoencephalography (MEG). All patients had BECRS diagnosis with typical seizures and electroencephalographic findings and five patients had minor psychomotor deficits. MEG was recorded over both parieto-temporal regions using a 2x37-channel biomagnetic system. The collected data were digitally bandpass-filtered (2-6, 14-30, or 1-70 Hz) to analyze slow- and fast-wave magnetic activities and rolandic spikes. Slow-wave activity was increased in four hemispheres of three patients. Increased fast-wave activity was found in all five patients with minor neuropsychological deficits. The presence of increased fast-wave magnetic brain activity appeared to cause functional anomalies in the higher brain function processes. In the spike analysis, the dipoles of rolandic spikes which constantly manifested anterior positivity in direction were concentrated in the superior rolandic region in four cases and the inferior rolandic region in three cases. The localizations of increased slow- and fast-wave activities were identical with those of the spikes. The seizure profiles were frequently characterized by the spike locations. Source localizations of the focal brain activities and rolandic spikes by MEG will contribute to the different diagnosis and pathophysiological elucidation of BECRS.

Functional and metabolic analysis of cerebral ischemia using magnetoencephalography and proton magnetic resonance spectroscopy.

The details of the relationship between brain function and metabolism in brain infarcts have not been studied. Using magnetoencephalography (MEG) and proton magnetic resonance spectroscopic imaging (1H MRSI), we localized sources of abnormal magnetic activities in ischemic brain regions and biochemical changes in suspected lesions showing pathological characteristics. Twelve patients with ischemic stroke were examined and the results of MEG and 1H MRSI were superimposed onto the corresponding MR images. The signal intensities of N-acetyl (NA) and lactate (Lac) were measured in the lesions with highly concentrated dipoles of slow wave activity. Eleven of 12 cases had increased slow wave activity in the cortical areas adjacent to the infarcts; 1 case was excluded because the infarct was too small (<1 cm in diameter). The signal intensity of NA in the regions with the highest slow wave activity was significantly reduced and was well correlated with the dipole density of slow waves. Though Lac was mildly accumulated in the lesions, the Lac level had no correlation with slow wave magnetic activity. The remaining and metabolically active cortical tissue showing NA signal produced the abnormal slow wave activity under lactic acidosis (mild accumulation of Lac).

Mechanical allodynia in postherpetic neuralgia: evidence for central mechanisms depending on nociceptive C-fiber degeneration.

In 12 zoster patients who had developed postherpetic neuralgia with dynamic mechanical allodynia and in six zoster patients who had recovered without pain, the functional role of nociceptive C-fibers in allodynia was assessed by quantifying axon reflex reactions induced by histamine iontophoresis within allodynic regions and in their contralateral sites. In patients with postherpetic neuralgia, histamine responses were reduced or abolished within allodynic areas, indicating degeneration of nociceptive C-fibers. In patients who recovered without pain, histamine responses were bilaterally identical, indicating complete regeneration of nociceptive C-fibers. These results demonstrate that sensitized nociceptive C-fibers are not involved in signaling and maintenance of allodynia. Alteration in CNS processing may reorganize synaptic ties between central pain-signaling pathways and mechanoreceptive A beta-fibers depending on afferent C-fiber degeneration rather than ongoing C-fiber input.

Axon-reflex reactions in affected and homologous contralateral skin after unilateral peripheral injury of thoracic segmental nerves in humans.

Transection and regeneration of a rat peripheral nerve on one side reduces the ability of the contralateral nerve to evoke plasma extravasation after antidromic excitation of afferent C-fibers induced by electrical nerve stimulation (afferent axon reflex). An unknown transneuronal signalling substance was postulated. In humans, axon-reflex vasodilatation was studied using cutaneous iontophoresis of histamine for C-fiber stimulation and laser Doppler flowmetry for measuring vasodilatation. As a model of peripheral nerve lesion with regeneration, patients with severe unilateral zoster neuropathy of thoracic segmental nerves were examined. Axon-reflex reactions were considerably impaired within the affected dermatome compared with the unaffected side and compared with controls. In contrast, no significant differences could be found between the unaffected corresponding sites of patients and similar dermatomes of healthy controls, indicating that this type of nerve injury does not influence the ability of the contralateral nerve to evoke axon-reflex vasodilatation.

Postherpetic neuralgia. Are C-nociceptors involved in signalling and maintenance of tactile allodynia?

Under normal conditions acute stimulation and sensitization of polymodal nociceptive C-fibres cause pain and, due to afferent axon reflex activation, a local skin vasodilatation, flare reaction and skin temperature increase. Two questions arise: (i) Do sensitized C-nociceptors signal allodynia in chronic postherpetic neuralgia? (ii) If not, does ongoing peripheral nociceptive C-fibre input maintain a central process that accounts for allodynia? Ten patients with postherpetic neuralgia and tactile allodynia and 10 control subjects were studied using a laser Doppler perfusion monitor. Peripheral nociceptive C-fibre function was assessed by quantitative measurement of the axon reflex vasodilatation and flare reaction induced by histamine iontophoresis and compared with non-neural vasodilatation induced by local skin heating. Resting skin temperature, skin resistance and resting skin blood flow were the same in the allodynic area and the contralateral homologous skin area. The histamine responses (vasodilatation and flare) were significantly reduced or nearly abolished in the allodynic area compared with the contralateral side, whereas the temperature-dependent vasodilatation in patients and the histamine responses in healthy controls showed no side differences. C-fibre mediated pain and itch sensations were also decreased in the allodynic area. These findings indicate a considerable impairment of cutaneous nociceptive C-fibre function in the allodynic area. Allodynic stimuli of 20 s did not cause any local blood flow change. Impairment of C-fibre function was positively correlated with intensity of neuropathic pain. We conclude that sensitized nociceptive C-fibres are not involved in signalling allodynia. Changes in CNS processing may occur after zoster infection that strengthen the synaptic ties between central pain signalling pathways and low-threshold mechanoreceptors with A beta-fibres. This altered central processing is not maintained by ongoing cutaneous nociceptive C-fibre input, at least in some patients with postherpetic neuralgia. On the contrary, an anatomical synaptic reorganization depending on afferent C-fibre degeneration seems to be more likely, particularly in advanced stages of postherpetic neuralgia.