[Functional imaging of brain tumors].
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Biomedical subjects
Publications and source records attributed to J Huttunen.
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The influence of neocortical muscarinic transmission on auditory-evoked 40-Hz magnetic response was studied in 13 healthy subjects in a double-blind randomized cross-over design. Either a centrally (scopolamine hydrobromide, 0.3 mg, i.v.) or a peripherally (glycopyrrolate, 0.2 mg, i.v.) acting antagonist of muscarinic transmission was administered during two sessions of magnetoencephalographic recording of 40-Hz response elicited by monaural tones. Scopolamine significantly (P < 0.01) augmented the 40-Hz magnetic response over the hemispheres ipsi- and contralateral to the ear stimulated. This finding suggests muscarinic modulation of the auditory evoked transient 40-Hz response.
BACKGROUND: Dietary components may be both causal and protective in cases of pancreatic carcinoma, but the preventive potential of single constituents has not been evaluated. The authors report the effects of alpha-tocopherol and beta-carotene supplementations on the rates of incidence of and mortality from pancreatic carcinoma in a randomized, controlled trial. METHODS: The 29,133 participants in the Alpha-Tocopherol Beta-Carotene Cancer Prevention (ATBC) Study were male smokers who were ages 50-69 years at the time they were randomized into 1 of the following 4 intervention groups: dl-alpha-tocopherol (AT; 50 mg/day), beta-carotene (BC; 20 mg/day), both AT and BC, and placebo. The daily supplementation lasted for 5-8 years. Incident cancers were identified through the national Finnish Cancer Registry and death certificates of the Statistics Finland. Results were analyzed by supplementation with Cox regression models. RESULTS: Effects of both supplementations were statistically nonsignificant. The rate of incidence of pancreatic carcinoma was 25% lower for the men who received beta-carotene supplements (n = 38) compared with the rate for those who did not receive beta-carotene (n = 51) (95% CI, -51% to 14%). Supplementation with alpha-tocopherol (n = 51) increased the rate of incidence by 34% (95% CI, -12% to 105%) compared with the rate for those who did not receive alpha-tocopherol. Mortality from pancreatic carcinoma during the follow-up, adjusted for stage and anatomic location of the tumor, was 19% (95% CI, -47% to 26%) lower among those who received beta-carotene and 11% (95% CI, -28% to 72%) higher among those who received alpha-tocopherol as compared with those who did not receive supplementation. CONCLUSIONS: Supplementation with beta-carotene or alpha-tocopherol does not have a statistically significant effect on the rate of incidence of pancreatic carcinoma or the rate of mortality caused by this disease.
The amplitudes of many scalp-recorded evoked potential (EP) deflections are higher in females than in males, and in elderly than in young subjects. Since EPs critically depend on the electric conductivity of the cranium, it is not known whether these differences reflect age- and gender-dependent changes in the intensity of neuronal activation, or changes in the volume conductor. Evoked magnetic fields are not significantly affected by the conductivities of the cranial tissues and therefore reflect more directly the neuronal activation than EPs. We report here on the effects of age and gender on somatosensory evoked fields (SEFs) from the primary somatosensory cortex (SI) in 43 healthy subjects (21 males) aged from 20 to 73 years (males 51+/-18 years, females 51+/-14 years). The intensity of neuronal activation was estimated with equivalent current dipoles (ECDs) found at the peaks of the N20m, P35m and P60m deflections from the left SI after right median nerve stimulation. The peak latencies of N20m and P35m (but not of P60m) were shorter in females than in males. The N20m latency was positively correlated with age in males, but otherwise the latencies did not correlate with age. The ECD amplitudes did not differ between males and females for any of the deflections. The N20m ECD strength showed a significant positive correlation (r=0.39, p<0.01) with age while P35m and P60m ECD strengths did not. The results thus did not disclose gender differences in the activation strengths of the somatosensory cortex, implying that such differences in evoked potentials may possibly be due to gender differences in the volume conductor. On the other hand, the results suggest a slight age-related increase in cortical excitability.
To study the influence of central cholinergic muscarinic transmission on human cortical middle-latency auditory evoked magnetic fields (MAEF), centrally acting antagonist scopolamine hydrobromide (0.3 mg, i.v.), and peripheral muscarinic receptor antagonist glycopyrrolate (0.2 mg, i.v.), were administered to 13 healthy subjects in a double-blind randomized cross-over design. MAEF, measured with whole-head magnetoencephalography (MEG), were elicited with clicks applied at 10-Hz rate to the left ear. The amplitudes of N(b)m and P(a)m responses were augmented by scopolamine (P < 0.01 and P < 0.08). These effects were about equally strong for responses from ipsi- and contralateral auditory cortices. Thus, the present MEG findings revealed specific modulation of cortical generators of middle-latency auditory evoked responses by muscarinic transmission. These findings might be associated with auditory processing deficits observed in dementias with cholinergic disturbances.
We combined information from functional magnetic resonance imaging (fMRI) and magnetoencephalography (MEG) to assess which cortical areas and in which temporal order show macroscopic activation after right median nerve stimulation. Five healthy subjects were studied with the two imaging modalities, which both revealed significant activation in the contra- and ipsilateral primary somatosensory cortex (SI), the contra- and ipsilateral opercular areas, the walls of the contralateral postcentral sulcus (PoCS), and the contralateral supplementary motor area (SMA). In fMRI, two separate foci of activation in the opercular cortex were discerned, one posteriorly in the parietal operculum (PO), and one anteriorly near the insula or frontal operculum (anterior operculum, AO). The activation sites from fMRI were used to constrain the solution of the inverse problem of MEG, which allowed us to construct a model of the temporal sequence of activation of the different sites. According to this model, the mean onset latency for significant activation at the contralateral SI was 20 msec (range, 17-22 msec), followed by activation of PoCS at 23 msec (range, 21-25 msec). The contralateral PO was activated at 26 msec (range, 19-32 msec) and AO at 33 msec (range, 22-51 msec). The contralateral SMA became active at 36 msec (range, 24-48 msec). The ipsilateral SI, PO, and AO became activated at 54-67 msec. We conclude that fMRI provides a useful means to constrain the inverse problem of MEG, allowing the construction of spatiotemporal models of cortical activation, which may have significant implications for the understanding of cortical network functioning.
It is well established that voluntary hyperventilation (HV) slows down electroencephalographic (EEG) rhythms. Little information is available, however, on the effects of HV on cortical responses elicited by sensory stimulation. In the present study, we recorded auditory evoked potentials (AEPs) and magnetic fields (AEFs), and somatosensory evoked magnetic fields (SEFs) from healthy subjects before, during, and after a 3- to 5-min period of voluntary HV. The effectiveness of HV was verified by measuring the end-tidal CO2 levels. Long-latency (100-200 ms) AEPs and long-latency AEFs originating at the supratemporal auditory cortex, as well as long-latency SEFs from the primary somatosensory cortex (SI) and from the opercular somatosensory cortex (OC), were all reduced during HV. The short-latency SEFs from SI were clearly less modified, there being, however, a slight reduction of the earliest cortical excitatory response, the N20m deflection. A middle-latency SEF deflection from SI at about 60 ms (P60 m) was slightly increased. For AEFs and SEFs, the center-of-gravity locations of the activated neuronal populations were not changed during HV. All amplitude changes returned to baseline levels within 10 min after the end of HV. The AEPs were not altered when the subjects breathed 5% CO2 in air in a hyperventilation-like manner, which prevented the development of hypocapnia. We conclude that moderate HV suppresses long-latency evoked responses from the primary projection cortices, while the early responses are less reduced. The reduction of long-latency responses is probably mediated by hypocapnia rather than by other nonspecific effects of HV. It is suggested that increased neuronal excitability caused by HV-induced hypocapnia leads to spontaneous and/or asynchronous firing of cortical neurones, which in turn reduces stimulus-locked synaptic events.
We recorded somatosensory evoked magnetic fields (SEFs) to median nerve stimulation from 15 patients in the acute stage (1-15 days from the onset of the symptoms) of their first-ever unilateral stroke involving sensorimotor cortical and/or subcortical structures in the territory of the middle cerebral artery (MCA). Neuronal activity corresponding to the peaks of the N20m, P35m and P60m SEF deflections from the contralateral primary somatosensory cortex (SI) was modelled with equivalent current dipoles (ECDs), the locations and strengths of which were compared with those of an age-matched normal population. Four patients with pure motor stroke had symmetric SEFs. In one of the 4 patients with pure sensory stroke, and in 5 of the 7 patients with sensorimotor paresis, the SEFs were markedly attenuated or missing. All except one patient with abnormal SEFs had deficient two-point discrimination ability; especially the attenuation of N20m was more clearly correlated with two-point discrimination than with joint-position or vibration senses. Of the different SEF deflections, P35m and P60m were slightly more sensitive indicators of abnormality than N20m, the former being affected in two patients with symmetric N20m. Three patients with pure sensory stroke and lesions in the opercular cortex had normal SEFs from SI. We conclude that the SEF deflections N20m, P35m and P60m from SI are related to cutaneous sensation, in particular discriminative to touch. The results also demonstrate that basic somatosensory perception can be affected by lesions in the opercular cortex in patients with functionally intact SI.
OBJECTIVE: To explore the applicability of the Depression Scale (DEPS), a screening instrument for detecting depression in primary health care, in schizophrenia. METHOD: The DEPS was compared with the Calgary Depression Scale (CDS) among 63 patients with schizophrenia. RESULTS: Using the CDS as a gold standard, the positive and negative predictive values of the DEPS for the diagnosis of depression were 41% and 97%, respectively. The correlation between the total CDS scores and the total DEPS scores was 0.73. CONCLUSION: The DEPS appears to be useful for screening depression among schizophrenic patients, but the positive diagnosis must be confirmed with a clinical interview.
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The objective of the present study was to evaluate the normal interhemispheric variability of the locations and activation strengths of the somatosensory cortices. Somatosensory evoked magnetic fields (SEFs) were recorded with a 122-channel magnetometer in 23 healthy subjects (mean age 57 years) to stimulation of left and right median nerves. Equivalent current dipole (ECD) strengths and locations were determined for the main SEF deflections at the contralateral primary sensorimotor (SMI) and secondary somatosensory (SIIc) cortices. In a Cartesian co-ordinate system, defined by the preauricular points and the nasion, the SMI sources were slightly but significantly more laterally and anteriorly located in the right than in the left hemisphere. No systematic co-ordinate asymmetries were found for the SIIc sources. In individual subjects, the interhemispheric differences in the ECD co-ordinates averaged less than 6 mm at both SMI and SIIc. The group means of the source strengths did not differ between the hemispheres, but individual differences were on average 20% for the SMI and 65% for the SIIc sources. We conclude that at the individual level, the median nerve SEFs from SMI can be used to detect abnormally large interhemispheric asymmetries of source locations in the centimetre scale.
The present study evaluated neurophysiologic function of the primary sensorimotor cortex in juvenile neuronal ceroid lipofuscinosis. A 122-channel magnetometer, which allowed studies of the somatosensory system in millimeter and millisecond precision, was used to record somatosensory evoked magnetic fields to median nerve stimulation from 10 patients and their matched control subjects. In both patients and controls, the somatosensory evoked magnetic fields from primary sensorimotor area typically consisted of N20m, P35m, and P60m deflections. In the patients, N20m was significantly delayed, whereas P35m peaked earlier than in the control subjects. The source strengths for N20m and P35m were greater in the patients than in the controls. Both deflections showed a significant positive correlation with the disease duration: the sources were stronger in the older patients than in the younger ones. P60m deflections were normal or reduced in the patients. The results indicated increased thalamocortical excitability in the sensorimotor cortex in juvenile neuronal ceroid lipofuscinosis.
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The functional significance of the second somatosensory cortex (SII) is poorly understood. However, lesion and cortical stimulation studies indicate that SII may be involved in sensory aspects of tactile learning and in movement control. In the present study, we explored a possible role of SII in sensorimotor integration in humans using a multichannel magnetometer. Somatosensory evoked fields (SEFs) from SII to electrical stimulation of left and right median nerves were recorded in six healthy volunteers during rest and in different test conditions. Continuous cutaneous stimulation of the right hand or face reduced the SEFs to both left and right median nerve stimulation. Right-sided finger movements increased the SEFs to right, but not left, median nerve stimulation. The responses were equally enhanced by simple finger flexion movement and by a complex finger sequence. The suppression of SEFs by competing cutaneous inputs from different areas of the body indicates that the neurones underlying the responses receive inputs from large, bilateral receptive fields. The enhancement of sensory reactions to signals from the actively moving limb but not to those from the opposite limb indicates a spatial tuning of the SII neurones to behaviourally relevant input channels, also suggesting that SII is important for the integration of sensory information to motor programmes.
Cerebral responses evoked by peripheral stimuli are known to depend critically on the interstimulus interval (ISI). Here we report on the effects of ISI on somatosensory evoked magnetic fields (SEFs) to right median nerve stimulation, obtained in 9 healthy adults with ISIs of 0.15 0.3, 1,3 and 5 s. At the contralateral (left) primary sensorimotor cortex (SMI), the first cortical response, N20m, was stable between the ISIs 0.3 and 5 s, but slightly attenuated at the shortest ISI of 0.15 s. In contrast, the P35m and P60m deflections were very sensitive to changes of the ISI, declining steadily with shortening of the ISI throughout the entire range. These deflections were frequently undetectable at the shortest ISI of 0.15 s. Concomitant with the reductions of P35m and P60m, an N45m deflection was enhanced toward the short ISIs. Responses from second somatosensory cortex (SII) and posterior parietal cortex (PPC) were seen only with ISIs of 1 s or greater, being strongest at the 5 s ISI. Based on known effects of the ISI on intracellular evoked potentials, we present the following tentative model for the generation mechanism of the SMI response: N20m represents early excitatory postsynaptic potentials (EPSPs), P35m early inhibitory postsynaptic potentials (IPSPs), N45m secondary EPSPs and P60m late IPSPs in pyramidal neurones of area 3b. For practical purposes, SEFs from SMI can be obtained with short ISIs, while responses from SII and PPC require an ISI of at least 1 s.
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