PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Sensorimotor Cortex”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources

Altered baseline brain activity in children with ADHD revealed by resting-state functional MRI.

In children with attention deficit hyperactivity disorder (ADHD), functional neuroimaging studies have revealed abnormalities in various brain regions, including prefrontal-striatal circuit, cerebellum, and brainstem. In the current study, we used a new marker of functional magnetic resonance imaging (fMRI), amplitude of low-frequency (0.01-0.08Hz) fluctuation (ALFF) to investigate the baseline brain function of this disorder. Thirteen boys with ADHD (13.0+/-1.4 years) were examined by resting-state fMRI and compared with age-matched controls. As a result, we found that patients with ADHD had decreased ALFF in the right inferior frontal cortex, [corrected] and bilateral cerebellum and the vermis as well as increased ALFF in the right anterior cingulated cortex, left sensorimotor cortex, and bilateral brainstem. This resting-state fMRI study suggests that the changed spontaneous neuronal activity of these regions may be implicated in the underlying pathophysiology in children with ADHD.

Adolescent↗

Episodic neonatal hypoxia evokes executive dysfunction and regionally specific alterations in markers of dopamine signaling.

Perinatal ischemic-anoxic and prolonged anoxic insults lead to impaired dopaminergic signaling and are hypothesized to contribute, at least in part, to the pathogenesis of disorders of minimal brain dysfunction such as attention-deficit hyperactivity disorder. We hypothesized that subtle intermittent hypoxic insults, occurring during a period of critical brain development, are also pathogenic to dopaminergic signaling, thereby contributing to behavioral and executive dysfunction. Between postnatal days 7 and 11, rat pups were exposed to either 20-s bursts of isocapnic hypoxic gas, compressed air, or were left undisturbed with the dam. On postnatal days 23 pups were instrumented with electroencephalographic/electromyographic electrodes and sleep-wake architecture was characterized. Locomotor activity was assessed between postnatal days 35 and 38, learning, and working memory evaluated between postnatal days 53 and 64. Rats were killed on postnatal day 80 and tyrosine hydroxylase, vesicular monoamine transporter, dopamine transporter, and dopamine D1 receptors were quantified in the prefrontal cortex, primary sensorimotor cortex, and precommissural striatum by Western blot analyses. Post-hypoxic pups spent less time awake and more time in rapid-eye-movement sleep during the lights-on phase of the circadian cycle, were hyperlocomotive, and expressed impaired working memory. Striatal expression of vesicular monoamine transporter and D1 receptor proteins were increased in post-hypoxic rats, consistent with depressed dopaminergic signaling. These observations lead to the intriguing hypothesis that intermittent hypoxia occurring during a period of critical brain development evokes behavioral and neurochemical alterations that are long lasting, and consistent with disorders of minimal brain dysfunction.

Animals↗

Effects of phencyclidine (PCP) and MK 801 on the EEGq in the prefrontal cortex of conscious rats; antagonism by clozapine, and antagonists of AMPA-, alpha(1)- and 5-HT(2A)-receptors.

1. The electroencephalographic (EEG) effects of the propsychotic agent phencyclidine (PCP), were studied in conscious rats using power spectra (0 - 30 Hz), from the prefrontal cortex or sensorimotor cortex. PCP (0.1 - 3 mg kg(-1) s.c.) caused a marked dose-dependent increase in EEG power in the frontal cortex at 1 - 3 Hz with decreases in power at higher frequencies (9 - 30 Hz). At high doses (3 mg kg(-1) s.c.) the entire spectrum shifted to more positive values, indicating an increase in cortical synchronization. MK 801 (0.05 - 0.1 mg kg(-1) i.p.) caused similar effects but with lesser changes in power. 2. In contrast, the non-competitive AMPA antagonists GYKI 52466 and GYKI 53655 increased EEG power over the whole power spectrum (1 - 10 mg kg(-1) i.p.). The atypical antipsychotic clozapine (0.2 mg kg(-1) s.c.) synchronized the EEG (peak 8 Hz). The 5-HT(2A)-antagonist, M100907, specifically increased EEG power at 2 - 3 Hz at low doses (10 and 50 microg kg(-1) s.c.), whereas at higher doses (0.1 mg kg(-1) s.c.) the profile resembled that of clozapine. 3. Clozapine (0.2 mg kg(-1) s.c. ), GYKI 53655 (5 mg kg(-1) i.p.), prazosin (0.05 and 0.1 mg kg(-1) i.p.), and M100907 (0.01 and 0.05 mg kg(-1) s.c.) antagonized the decrease in power between 5 and 30 Hz caused by PCP (1 mg kg(-1) s.c.), but not the increase in power at 1 - 3 Hz in prefrontal cortex.

Animals↗

Aging alters the multichemical networking profile of the human brain: an in vivo (1)H-MRS study of young versus middle-aged subjects.

In our most recent study of normal aging, we found decreased concentration of multiple chemicals in the brain of middle-aged subjects, as compared with younger subjects using in vivo proton magnetic resonance spectroscopy ((1)H-MRS). We hypothesized that these age-dependent differences in brain chemistry changes might be a reflection of the multichemical-networking-profile (MCNP) changes during aging. Using (1)H-MRS and correlation analysis, we examined the patterns of regional chemical levels and MCNP within and across multiple brain regions for all nine chemicals of (1)H-MR spectra. The brain chemistry changes and MCNP patterns were compared between 21 young (19--31-year-old) and 31 middle-aged (40--52-year-old) normal volunteers. Middle-aged subjects demonstrated a significant decrease of chemical levels in the prefrontal cortex and sensorimotor cortex (SMC), as compared with the young age group. Of these, neurotransmitters GABA and glutamate in the dorsolateral prefrontal cortex (DLPFC) were altered the most. We also found a significant increase of overall chemical correlation strength in MCNP within and across all studied brain regions with increased age. These changes were caused by alterations in the pattern of negative chemical connectivity across brain regions, which become weaker (less negative) in middle-aged subjects. The interregional chemical connectivity for the cingulate cortex, SMC and the thalamus was changed the most with increased age. Increased levels of chemical correlation strength across brain regions in aging were found for most chemicals studied (including neurotransmitters GABA and glutamate), and not for N-acetyl aspartate. These age-related differences in the connectivity of neurotransmitters were not region dependent. The results suggest that aging is associated with changes of the regional brain chemistry and the brain MCNP. The latter process may reflect an adaptive or compensatory response (possibly related to the elongation of dendrites with aging) to reduced levels of regional brain chemicals. The (1)H-MRS approach proposed here can be used as a valuable tool in the study of the brain chemistry, MCNP and their relationships in normal and abnormal aging.

Adult↗

C-fos expression during vocal mobbing in the new world monkey Saguinus fuscicollis.

In order to find brain areas involved in the vocal expression of emotion, we compared c-fos expression in three groups of saddle-back tamarins (Saguinus fuscicollis). One group, consisting of three animals, was made to utter more than 800 mobbing calls by electrical stimulation of the periaqueductal grey of the midbrain (PAG). A second group, consisting of two animals, was stimulated in the PAG with the same intensity and for the same duration as the first group but at sites that did not produce vocalization. These sites lay somewhat medial to the vocalization-eliciting sites. A third group, consisting of two animals, was stimulated at vocalization-eliciting sites in the PAG but with an intensity below vocalization threshold. Fos-like immunoreactivity that was found in the vocalizing but not in the non-vocalizing animals was located in the dorsomedial and ventrolateral prefrontal cortex, anterior cingulate cortex, ventrolateral premotor cortex, sensorimotor face cortex, insula, inferior parietal cortex, superior temporal cortex, claustrum, entorhinal and parahippocampal cortex, basal amygdaloid nucleus, anterior and dorsomedial hypothalamus, nucleus reuniens, lateral habenula, Edinger-Westphal nucleus, ventral and dorsolateral midbrain tegmentum, nucleus cuneiformis, sagulum, pedunculopontine and laterodorsal tegmental nuclei, ventral raphe, periambigual reticular formation and solitary tract nucleus. For some of these structures (e.g. anterior cingulate cortex and periambigual reticular formation), there is evidence also from electrical stimulation, lesioning and single-unit recording studies that they are involved in vocal control. For other structures (e.g. lateral habenula, Edinger-Westphal nucleus), the available evidence speaks against such a role. Fos activation in these cases is probably related to non-vocal reactions accompanying the electrically elicited vocalizations. A third group of structures consists of areas for which a role in vocal control cannot be excluded but for which the present study presents the first evidence for such a role (e.g. claustrum and sagulum). These structures deserve further studies using more specific methods.

Animals↗

Empathy for pain involves the affective but not sensory components of pain.

Our ability to have an experience of another's pain is characteristic of empathy. Using functional imaging, we assessed brain activity while volunteers experienced a painful stimulus and compared it to that elicited when they observed a signal indicating that their loved one--present in the same room--was receiving a similar pain stimulus. Bilateral anterior insula (AI), rostral anterior cingulate cortex (ACC), brainstem, and cerebellum were activated when subjects received pain and also by a signal that a loved one experienced pain. AI and ACC activation correlated with individual empathy scores. Activity in the posterior insula/secondary somatosensory cortex, the sensorimotor cortex (SI/MI), and the caudal ACC was specific to receiving pain. Thus, a neural response in AI and rostral ACC, activated in common for "self" and "other" conditions, suggests that the neural substrate for empathic experience does not involve the entire "pain matrix." We conclude that only that part of the pain network associated with its affective qualities, but not its sensory qualities, mediates empathy.

Adult↗

PET imaging of serotonin type 2A receptors in late-life neuropsychiatric disorders.

OBJECTIVE: To determine whether there are abnormalities in the in vivo status of the serotonin type 2A (5-HT2A) receptor in late-life depression and Alzheimer's disease, the authors used positron emission tomography (PET) to assess patients with these two conditions and healthy subjects. METHOD: PET was performed by using [18F]altanserin to evaluate 5-HT2A receptor binding in 11 elderly patients with depression (four men, seven women; mean age = 65.0 years, SD = 5.5); nine Alzheimer's disease patients, including three with concurrent depression (two men, seven women; mean age = 69.7 years, SD = 5.0); and 10 age-matched healthy subjects (four men, six women; mean age = 69.8 years, SD = 5.0). Partial-volume correction of regional specific binding estimates was performed by using a method based on magnetic resonance imaging. RESULTS: No significant abnormalities in [18F]altanserin binding (binding potential) were observed in the patients with late-life depression, and no effect of depression on binding potential was present within the Alzheimer's disease group. However, the patients with Alzheimer's disease had significantly lower binding than the normal subjects in several brain regions, including the anterior cingulate, prefrontal cortex, and sensorimotor cortex. CONCLUSIONS: These results suggest that the 5-HT2A receptor is differentially affected in late-life depression and Alzheimer's disease, a finding that has implications for the etiological basis of mood and cognitive features of neuropsychiatric disorders of late life.

Age Factors↗

Functional magnetic resonance imaging study of writer's cramp.

BACKGROUND: Writer's cramp is a type of task specific idiopathic focal dystonia and has an incompletely understood pathophysiology. The present study utilized functional magnetic resonance imaging (fMRI) to investigate what type of brain activity correlates with writer's cramp and its physiological mechanism. METHODS: Ten patients with writer's cramp were age and gender matched with ten healthy control subjects in a block design. Subjects were scanned by fMRI while performing three consecutive, visually instructive, tasks with MR Vision 2000: (1) suppositional writing, (2) writing with finger and (3) writing with a pencil. Data was analysed using AFNI software for groups of patients and controls. RESULTS: The patients with writer's cramp showed significant activations of contralateral basal ganglion (especially the putamen), motor cortex (primary sensorimotor cortex, supplementary motor cortex, premotor cortex) and ipsilateral cerebellar hemisphere in writing with a pencil compared with controls; whereas there was no obvious difference between patients and controls during writing with finger. Furthermore, these differences exist in the subtractive activated maps for "writing with a pencil" minus "writing with finger" of patients, when the activation of subcortical area and insula in controls disappeared. CONCLUSIONS: Abnormal activations of contralateral basal ganglion, motor cortex and ipsilateral cerebellar hemisphere of the patients with writer's cramp suggest dysfunction of basal ganglion and subcortical-cortical loop might play a pathophysiological role in writer's cramp.

Adult↗

Postmortem increases in GABA receptor binding to membranes of cat central nervous system.

GABA receptor binding in fifteen regions of cat central nervous system was investigated immediately postmortem and at twelve, twenty-four, and 72 hours postmortem. In each of the supraspinal areas studied, GABA binding increased with time-after-death. Changes after 24 hours occurred in the cerebellum, the visual cortex, the sensorimotor cortex, and the amygdala where more than a two-fold increase in binding was observed. Increases were also noted in the thalamus, caudate nucleus, hippocampus, and hypothalamus. The results suggest that caution should be exercised in the interpretation of GABA binding data obtained from human brains that have not been treated in a similar postmortem manner.

Animals↗

Comparison of technetium-99m-HMPAO and technetium-99m-ECD cerebral SPECT images in Alzheimer's disease.

UNLABELLED: SPECT has shown increasing promise as a diagnostic tool in Alzheimer's disease (AD). Recently, a new SPECT brain perfusion agent, 99mTc-ethyl cysteinate dimer (99mTc-ECD) has emerged with purported advantages in image quality over the established tracer, 99mTc-hexamethylpropyleneamine oxime (99mTc-HMPAO). This research aimed to compare cerebral images for 99mTc-HMPAO and 99mTc-ECD in discriminating patients with AD from control subjects. METHODS: Twenty-four AD patients (mean age +/- s.d. = 68.9 +/- 8.2 yr) and 13 healthy subjects (68.4 +/- 8.0 yr) were scanned sequentially with 20 mCi of each tracer using the CERASPECT system within 1 mo. Scanning began on average 11.5 +/- 2.8 min after 99mTc-HMPAO injection and 41.8 +/- 10.1 min after 99mTc-ECD. A ratio, R, was derived of count densities in "typically affected" brain structures (parietal and temporal association cortices) to "unaffected" structures (cerebellum, basal ganglia, thalamus, occipital cortex, and sensorimotor cortex). RESULTS: Analysis of variance revealed significant interaction between diagnostic group and radiopharmaceutical (F = 4.71; df = 1.35; p = 0.04), with 99mTc-ECD demonstrating better separation of R values between AD patients and control subjects than 99mTc-HMPAO. Receiver operating characteristic (ROC) analysis, revealed no significant difference in the ability of the two tracers to correctly classify AD patients and control subjects. Both tracers showed high diagnostic accuracy (99mTc-ECD: sensitivity = 100%, specificity = 92%; 99mTc-HMPAO: sensitivity = 100%, specificity = 85%). CONCLUSION: Technetium-99m-ECD shows greater contrast than 99mTc-HMPAO between affected and unaffected brain structures in AD when patients are compared to age-matched control subjects. Both tracers perform equally well in correctly classifying patients and control subjects.

Aged↗

Single- and multiple-event paradigms for identification of motor cortex activation.

BACKGROUND AND PURPOSE: The "single-event" technique has been used as an alternative to the "block-trial" method to detect activation that may be accompanied by head motion. The purpose of this study was to compare the two methods for measuring activation in the sensorimotor cortex secondary to motor tasks. METHODS: Functional MR imaging data were acquired from six participants as they performed tasks with their fingers, tongues, and toes in a block-trial and a single-event paradigm. For the block trial, the participant was instructed to perform the task when cued at a rapid self-timed rate for 15 seconds, alternating with 15 seconds of rest. Five periods of task performance and six rest periods were included in one acquisition. For the single-event method, the participant performed the task a single time every 15 seconds when cued by the investigator, for a total of 21 times. Using conventional parcellation methods, activation was detected by a cross-correlation technique and was classified as occurring in the sensorimotor cortex, supplementary motor area (SMA), or as nonspecific. Differences between the two acquisition paradigms were tested using the standard t test at a significance level of P < .05. RESULTS: Activation was identified by both the block-trial and the single-event methods for the finger task, for the tongue task, and inconsistently for the toe task. More motion artifact occurred in conjunction with the toe and tongue tasks than with the finger tasks. On average, more activated pixels were identified by the single-event method than by the block-trial method. For these motor tasks, however, a larger percentage of pixels detected by the block-trial method than by the single-event method were specific for the sensorimotor cortex or SMA as sites of activation. CONCLUSION: For the tongue and the toe movement tasks, which may produce some head motion artifacts, the single-event paradigm provides a useful alternative to the block-trial method for identifying the sensorimotor cortex or SMA. It does not achieve a greater percentage of activation within primary motor areas. For the finger movement task, which does not usually produce head motion artifacts, the block-trial method generally produced a greater percentage of activated pixels in the sensorimotor cortex or SMA than did the single-event method.

Adult↗

Recovery of forepaw gripping ability and reorganization of cortical motor control following cervical spinal cord injuries in mice.

Previous studies using a grip strength meter (GSM) revealed a loss of gripping ability following cervical hemisection injuries in mice, followed by partial recovery. Here, we assess whether normal gripping ability and the recovered gripping ability after cervical hemisection depend on the cerebral cortex. First, we assessed grip strength of both forepaws of 18-week-old C57Bl/6 mice before and after a left sensorimotor cortex lesion or right lateral hemisection at C5. Both lesions led to a complete loss of gripping ability by the right forepaw and caused only minor deficits in the left. After cortical lesions, gripping ability re-appeared at about 17 days post-injury, and grip strength recovered to near-normal levels by 24 days post-injury. After C5 hemisections, gripping ability re-appeared after 31 days post-injury in 50% of the mice. Follow-up experiments were then carried out in which 10-week-old mice received C4 hemisection injuries and were tested for 28 days; then mice received secondary lesions of the sensorimotor cortex ipsi- or contralateral to the hemisection. Younger mice with cervical hemisections recovered gripping ability between 12 and 28 days post-hemisection. Cortical lesions on the side contralateral to the hemisection led to a complete loss of recovered gripping ability in all mice; cortical lesions on the side ipsilateral to the hemisection also disrupted recovered gripping ability in some animals. Surprisingly, lesions of the cortex ipsilateral to the hemisection did not impair gripping ability of the contralateral (left) forepaw. Finally, we assessed the effects of a third lesion of whichever side of the sensorimotor cortex remained, so that the sensorimotor cortex was ablated bilaterally. Remarkably, gripping function by the forepaw contralateral to the original hemisection was completely unaffected, and the recovered gripping function by the forepaw ipsilateral to the hemisection was disrupted in only some of the animals. These results indicate a substantial reorganization of motor control of gripping function after cervical injuries in mice so that gripping ability by both forepaws becomes largely independent of cortical control.

Animals↗

Semisynthetic sphingolipids prevent protein kinase C translocation and neuronal damage in the perifocal area following a photochemically induced thrombotic brain cortical lesion.

A vascular thrombotic lesion localized to the rat sensorimotor cortex was produced following intravenous injection of the photosensitive dye rose bengal, and its activation with a small beam of high-intensity white light focused to the skull overlaying the sensorimotor cortex. In the sensorimotor cortex at various times after the triggering event, two contiguous brain regions with different degree(s) of neuronal damage can be distinguished: (1) a primary thrombotic ischemic core where the majority of cells are dead and (2) a penumbra region surrounding the core lesion in which a slower progressive neuronal degeneration is occurring. Importantly, in both brain regions the neuronal degeneration is associated with the activation and persistent translocation of protein kinase C (PKC) as indicated by an increase in 4-beta-3H-phorbol-12,13-dibutyrate (3H-PDBu) binding. Moreover, the demonstration that in the area penumbra the neuronal degeneration and the persistent translocation of PKC can be inhibited by a pretreatment with dizocilpine (i.e., MK-801) indicates that the dynamics of the progression of the neuronal degeneration are maintained by glutamate accumulating in the extraneuronal fluids. MK-801 additionally prevents the transcriptional activation of several immediate-early genes (IEGs) (e.g., c-fos) and their cognate third nuclear messenger (i.e., c-Fos) expression present in the hemisphere ipsilateral to the lesion. On the other hand, LIGA4 and LIGA20 derivatives of GM1 lysoganglioside reduce the membrane translocation of PKC and the neuronal damage in the penumbra area, but fail to change the increase of IEG expression in the cortex ipsilateral to the lesion.

Animals↗

Imaging of somatotopic representation of sensory cortex with intrinsic optical signals as guides for brain tumor surgery.

OBJECT: Intrinsic optical signals in response to somatosensory stimuli were intraoperatively recorded during brain tumor surgery. In the present study, the authors report on the use of this technique as an intraoperative guide for the safe resection of tumors adjacent to or within the sensorimotor cortex. METHODS: In 14 patients with tumors adjacent to or within the sensorimotor cortex, intrinsic optical signals in response to somatosensory stimuli were recorded by illuminating the brain surface with Xe white light and imaging the reflected light passing through a bandpass filter (605 nm). Results were compared with intraoperative recordings of sensory evoked potentials in all 14 patients and with noninvasive mapping modalities such as magnetoencephalography and positron emission tomography in selected patients. In all but two patients, the somatosensory optical signals were recorded on the primary sensory cortex. Optical signals elicited by stimulation of the first and fifth digits and the three branches of the trigeminal nerve were recorded at different locations on the sensory strip. This somatotopic information was useful in determining the resection border in patients with glioma located in the sensorimotor cortex. CONCLUSIONS: Optical imaging of intrinsic signals is a useful technique with superior spatial resolution for delineating the somatotopic representation of human primary sensory cortex. Furthermore, it can be used as an intraoperative monitoring tool to improve the safety and accuracy of resections of brain tumors adjacent to or within the sensorimotor cortex.

Adult↗

Gene expression profiling in the intact and injured brain following environmental enrichment.

An enriched environment promotes structural changes in both injured and intact brain and improves behavioral performance. In 2 different experimental approaches, the effects of enriched surroundings were analyzed utilizing DNA microarrays. First, gene expression patterns of the sensorimotor cortex and the hippocampus of noninjured adult rats with enriched housing were compared with analogous regions of rats kept in standard cages. Second, circumscribed infarcts affecting the forelimb area of the sensorimotor cortex were induced, and gene expression patterns of the non-necrotic ipsilesional as well as the contralesional homotopic cortex of rats (postlesionally enriched housing versus standard) were analyzed. In the intact brain, the hippocampus, which had 43 upregulations and 15 downregulations showed more changes than the sensorimotor cortex, which had 13 upregulations and 4 downregulations, indicating a greater responsiveness of the hippocampus to environmental stimuli. In the injured brain, enrichment led ipsilesionally to 28 downregulations and 14 upregulations, while in the contralesional cortex, upregulations prevailed with 46 upregulations and 13 downregulations. The larger number of genes responsive to enrichment in the contralesional cortex (59 gene regulations) as compared to the analogous area (i.e. sensorimotor cortex) of the intact brain (17 gene regulations) likely reflects increased susceptibility for plastic changes due to injury. With the exception of the perilesional cortex, similar functional groups of genes were differentially regulated in different brain regions/paradigms, suggesting basically similar molecular cascades being involved in reorganizing the brain following external stimuli. Many of the genes detected here correspond to molecular pathways known to be involved in neuroplasticity, whereas others provide new and hitherto unrecognized entry points.

Animals↗

Cortical function in amyotrophic lateral sclerosis. A positron emission tomography study.

Positron emission tomography was used to measure regional cerebral blood flow (rCBF) in 12 patients with amyotrophic lateral sclerosis (ALS) and six age-matched controls. Scans were performed at rest, and while subjects performed stereotyped and freely selected movements of a joystick with their right hand. Statistical parametric mapping was used to determine significant differences in rCBF between the two groups at rest and during activation. The ALS group showed no significant difference in global cerebral blood flow at rest compared with controls. However, rCBF at rest was significantly (P < 0.01) reduced in the ALS group in the primary sensorimotor cortex, the lateral premotor cortex, the supplementary motor area, the anterior cingulate cortex, the paracentral lobule and the superior and inferior parietal cortex. Comparison of the increase in rCBF caused by freely selected joystick movements over the resting state between the two groups of subjects showed significantly (P < 0.001) greater activation in ALS patients in the ventral third (face area) of the contralateral primary sensorimotor cortex and in the adjacent contralateral ventral premotor and parietal association cortices; significantly (P < 0.01) greater activation of the contralateral anterior insula and the ipsilateral anterior cingulate cortex (dorso-caudal area 24) was also present in ALS patients. When a comparison of the rCBF response to the free selection task with that to the stereotyped task was performed between the two groups of subjects, ALS patients showed significantly impaired (P < 0.01) activation of the rostral anterior cingulate cortex (area 32), medial prefrontal cortex (area 10), left parahippocampal gyrus and retrosplenial cortex. The pattern of reduced rCBF at rest in ALS patients probably reflects a combination of neuronal loss in all areas of cortex projecting through the pyramidal tract together with loss of projections from the sensorimotor cortex to the motor association areas. The expansion of the upper limb output zone of the sensorimotor cortex in ALS patients during contralateral upper limb movement may represent cortical reorganization in response to Betz cell loss or corticospinal tract disruption. Abnormal recruitment of non-primary motor areas may also represent functional adaptation to a corticospinal tract lesion. Focally impaired activation of the medial prefrontal cortex and parahippocampal gyrus in ALS patients during the process of internal generation of movement could underlie the frontal lobe cognitive deficits reported in previous neuropsychological studies of ALS.

Adult↗

Increase in focal concentration of deoxyhaemoglobin during neuronal activity in cerebral ischaemic patients.

BACKGROUND AND PURPOSE: Blood oxygenation level dependent contrast functional magnetic resonance imaging (BOLD-fMRI) has been applied to functional mapping in brain disorders, based on the assumption that normal adults and patients with brain disorders exhibit similar evoked cerebral blood oxygenation (CBO) changes. This study compared evoked CBO changes measured by near infrared spectroscopy (NIRS) with the activation mapping obtained by BOLD-fMRI in patients with cerebral ischaemia. METHODS: The study involved six normal adults and six patients with cerebral ischaemia. Hand grasping was performed as a motor task. All patients could perform the task similarly to the controls at the time of examination, but single photon emission computed tomography demonstrated low baseline cerebral blood flow and a decreased haemodynamic reserve in the primary sensorimotor cortex on the lesion side. Using NIRS, concentration changes of deoxyhaemoglobin (Deoxy-Hb), oxyhaemoglobin (Oxy-Hb), and total haemoglobin (Total-Hb) were measured in the primary sensorimotor cortex contralateral to the task. BOLD-fMRI signals were measured by 1.5 T magnetic resonance imaging using an echo-planar technique. Activation maps were calculated by statistical parametric mapping. RESULTS: In the controls, Deoxy-Hb decreased in association with increases of Oxy-Hb and Total-Hb in the primary sensorimotor cortex during the task. However, in the patients, Deoxy-Hb increased significantly from baseline, while Oxy-Hb and Total-Hb also increased, indicating the presence of rCBF increases in response to neuronal activation. BOLD-fMRI demonstrated only limited activation areas in the primary sensorimotor cortex on the lesion side. CONCLUSION: The CBO changes in patients with cerebral ischaemia differed from those of normal adults; Deoxy-Hb was increased in activation areas of the patients. This implies that BOLD-fMRI may overlook activation areas in the patients unless both increases and decreases of signal are taken into consideration.

Adult↗

Neuromagnetic fields accompanying unilateral and bilateral voluntary movements: topography and analysis of cortical sources.

Movement-related magnetic fields (MRMFs) accompanying left and right unilateral and bilateral finger flexions were studied in 6 right-handed subjects. Six different MRMF components occurring prior to, and during both unilateral and bilateral movements are described: a slow pre-movement readiness field (RF, 1-0.5 sec prior to movement onset); a motor field (MF) starting shortly before EMG onset; 3 separate "movement-evoked" fields following EMG onset (MEFI at 100 msec; MEFII at 225 msec; and MEFIII at 320 msec); and a "post-movement" field (PMF) following the movement itself. The bilateral topography of the RF and MF for both unilateral and bilateral movements suggested bilateral generators for both conditions. Least-squares fitting of equivalent current dipole sources also indicated bilateral sources for MF prior to both unilateral and bilateral movements with significantly greater strength of contralateral sources in the case of unilateral movements. Differences in pre-movement field patterns for left versus right unilateral movements indicated possible cerebral dominance effects as well. A single current dipole in the contralateral sensorimotor cortex could account for the MEFI for unilateral movements and bilateral sensorimotor sources for bilateral movements. Other MRMF components following EMG onset indicated similar sources in sensorimotor cortex related to sensory feedback or internal monitoring of the movement. The results are discussed with respect to the possible generators active in sensorimotor cortex during unilateral and bilateral movement preparation and execution and their significance for the study of cortical organization of voluntary movement.

Brain Mapping↗